Tag Archives: Posterior Cortical Atrophy

So does this mean that folks with an immune deficiency in complement C3 have some kind of protection against Alzheimer’s?

You might have autoimmune diseases and chest infections that take forever to clear, but possibly also less of your brain disappearing with age, if research on mice is relevant to people.

Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice

http://stm.sciencemag.org/content/9/392/eaaf6295

Readers of this blog from back in 2011-2012 could have predicted this, because I pretty-much predicted this with my immune hypothesis of synaesthesia and my immune hypothesis of Benson’s syndrome (a variety of dementia). I wonder how many lives could have been saved and cases of dementia prevented if the world of science had bothered to read my blog and taken my theories seriously back then and set to work finding a therapy that reduces levels of C3? How hard could that be? It happens naturally, so how hard could it be to engineer a similar process? Instead all I got for my ideas and blogging was synaesthesia researchers plagiarizing my ideas shamelessly in a speculative paper about synaesthesia (a mere triviality in the world of neuroscience compared with the tragic and expensive problem of dementia). And all this time funding for dementia research has been counted in the hundreds of millions of dollars and has given the public virutally nothing in the way of effective therapies. How much of that research funding do I get? Not one single frickin’ red cent, because I’m not a scientist. I’m just a housewife with ideas, and a blog.

 

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If synaesthesia is caused by low levels of complement, does that mean it is the opposite of schizophrenia?

The idea that schizophrenia is caused by brain dysfunction resulting from excessive synaptic pruning during the teenage years is certainly nothing new, I’ve been aware of it for many years and I think it is a winner, but the idea that this excessive pruning is triggered by higher than normal levels of complement appears to be new, although quite predictable in light of my immune hypothesis of synaesthesia which I published at this blog way back in 2012, even though, to be fair, at the time I was contrasting a variety of dementia (PCA or Benson’s syndrome) with synaesthesia, not schizophrenia. It is possibly worth noting though that schizophrenia was originally known as “dementia praecox” and might not be an entirely different thing to Bensons dementia in reality. I’ve written it before and I’ll repreat it again; I believe that Benson’s syndrome could be caused by excessive levels of complement, specifically C3 but I could be wrong in that specific suggestion. Regardless of the importance of the differences between Benson’s and schizophrenia, I’d still argue that this exciting theory about schizophrenia and high complement and over-pruning that is apparently supported by evidence is such a mirror-image of my theory about synaesthesia and low complement and under-pruning from 2012 that my theory could have been an influence on the schizophrenia researchers whose work has just been published in Nature, but I doubt that I got any credit.

It is exciting that progress is possibly being made into understanding and maybe even preventing schizophrenia, and it is about bloody time, (and how hard could it be to hinder the action of C4 or get rid of some of it, for heaven’s sake, to save some poor wretch’s brain and mind?) but now I’m left wondering what, if any, is the relationship between Benson’s syndrome and schizophrenia? My limited knowledge of Benson’s identifies only memory problems as a common feature of the two brain disorders, (and isn’t it interesting that I and more conventional synaesthesia researchers have linked synaesthesia with superiority in memory?) but I’m wondering if there is more in common between Sz and Benson’s than memory issues. I guess if I was really interested I’d turn to Google and PubMed to check whether someone has done a study of the immune system genetics of people who have Benson’s, but I have so many other less interesting things to do today. If no one has done such a study, then maybe they should, and then thank me for the tip.

 

Wilson, Clare Overactive brain pruning in teens could cause schizophrenia. New Scientist. January 27th 2016.

https://www.newscientist.com/article/2075495-overactive-brain-pruning-in-teens-could-cause-schizophrenia/

 

Aswin Sekar, Allison R. Bialas, Heather de Rivera, Avery Davis, Timothy R. Hammond et al. Schizophrenia risk from complex variation of complement component 4. Nature. January 27th 2016.

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature16549.html

 

C. Wright Is synaesthesia caused by low levels of complement? Is Benson’s syndrome (PCA) caused by too much complement C3? Could synesthesia and posterior cortical atrophy be considered in some way opposites? Am I a super=recognizer? June 7, 2012.

https://superrecognizer.wordpress.com/2012/06/07/is-synaesthesia-caused-by-low-levels-of-complement-is-bensons-syndrome-caused-by-too-much-complement-c3/

 

Radio show about Glenda Parkin living with dementia in suburb of Perth, Western Australia

Below are the details of a recent and very interesting radio interview on Perth public radio with Glenda and Bronte Parkin and Alzheimers WA CEO Rhonda Parker, focusing on Glenda’s experiences as a person who has a form of dementia that goes by a number of names including Benson’s syndrome, posterior cortical atrophy and PCA. This is not the first time that Glenda has shared her story with the media; she previously shared her story with Perth’s daily newspaper, the West Australian, in 2011 and she has recently been interviewed for the Community Newspaper Group.

I have unusual reasons to be grateful that Glenda has shared her story with the mass media. I happened upon her story in a copy of the West while I was enjoying coffee and one of those wonderfully greasy Sausage and Egg McMuffins in a McDonald’s restaurant in 2011, after dropping someone off to a selective school that offers students places based on high ability in the area of literacy and languages. I became intrigued by the fact that the particular type of dementia described in the article appeared to be a mirror-image of the pattern of intellectual gifts that appear to run in our family, associated with synaesthesia, a harmless, genetic, developmental and memory-enhancing condition that is caused by increased connectivity in the structure of the white matter of the brain. I wondered whether there could be an undiscovered developmental basis of Benson’s syndrome that works like the opposite of synesthesia, or could it be caused by some mature-age dysregulation of some chemical that regulates growth in the parts of the brain that seem to be hyper-developed in our family, and attacked, over-pruned or somehow damaged in Benson’s. I wrote about my ideas in this blog soon after. In 2012 my thinking on this theme took an important and exciting leap ahead when I happened across a brief article in New Scientist about research by Dr Beth Stevens on microglia, complement, synaptic pruning and elements of the immune system playing a central role in the development of the brain. I figured that one or maybe more of the complement chemicals could be the chemical that regulates growth or pruning in the parts of the brain that I had written about and attempted to identify in my 2011 blog post. I wrote a brief outline of these ideas at this blog in 2012 in an article that was archived by the Internet Archive Wayback Machine in 2012. In lat 2013 I got a big surprise when I saw my idea linking the immune system with synaesthesia as the main idea of a research paper published in a peer-reviewed neuroscience journal, and all without my permission! That’s another story….

I am sure that many people listening to this radio interview would be fascinated with or even skeptical of Glenda’s account of being able to see but not perceive letters on the cover of a book. Her eyesight is not the problem, the problem lies in the visual processing areas of her brain and because of this a lady who in her impressive career has been an author of books can no longer read text or interpret symbols. Seeing is as much done in the brain as it is done in the eye and optic nerves, and a person who has no apparent problem with their eyes can lose visual perception as the result of dementia or injury or stroke.

“Simple things can be very frustrating” – Glenda and Bronte Parkin on dementia. Mornings with Geoff Hutchison. 720 ABC Perth.
09/07/2014.
http://blogs.abc.net.au/wa/2014/07/simple-things-can-be-very-frustrating-glenda-and-bronte-parkin-on-dementia.html

Jarvis, Lucy Still making a contribution: retired educators share experience of living with dementia. Community Newspapers. 2015

Hiatt, Bethany Penrhos principal’s hardest battle.  West Australian. January 3, 2011. http://au.news.yahoo.com/thewest/a/-/mp/8588194/glenda-parkin/

Postscript March 10th 2015

The West Weekend liftout of the West Australian of February 14-15 2015 has a feature story about West Australians livng with dementia on pages 10-13. he story of Glenda and Bronte Parkin is included in that article and the content makes it clear that although Glenda Parkin has a diagnosis of Benson’s syndrome which has had a negative impact on her ability to recognize symbols, writing and objects, she can still somehow navigate her way in her neighbourhood. I find this interesting as some people who have prosopagnosia, which is an impairment in face memory, also have a similar impairment in visual memory of scenes or landscapes, and thus have serious problems with navigating their way through streets and neighbourhoods. I had thought that Benson’s syndrome, a type of dementia, and prosopagnosia, a developmental disability and also sometimes acquired from brain injury, must be in many ways similar in their manifestations, as they both feature disability in face recognition, but it appears that it is not safe to make assumptions and maybe each case of these two conditions should be considered unique. I do not recall reading about Glenda Parkin’s ability to recognize faces, so maybe I should assume it is still normal, along with her ability to recognize street-scapes and scenes.

Yeoman, William Open minds. West Weekend. p. 10-13 West Australian. February 14-15 2015.

 

Would you like to follow these steps?

First go the the Internet Archive (Wayback Machine):  https://archive.org/

Then copy and paste the web address of this blog into the search form that you will find there, removing the beginning bit, and click on “BROWSE HISTORY”:   https://superrecognizer.wordpress.com/

The results screen that comes up will show you how many times this blog has been archived by the Internet Archive over the years.

Click on the year 2012, then click on the date June 21st 2012.

The Internet Archive will display to you their archived record of the home page of this blog as recorded on June 21st 2012. You will see a blog coloured in green and blue with stories featuring photos of some sculptures seen around Perth, but the thing that you might (or might not) find interesting is the blog post that is third down the page which was first published on June 7th 2012. This is the blog post where I briefly but clearly published my ideas suggesting causal relationships between the human immune system and synaesthesia, and low levels of some of the complement immune chemicals and synaesthesia, all related to the regulation of developmental synaptic pruning and synaptic plasticity involving the activity of microglia, and in this post I also restated my previously-published speculation that the variety of dementia known as Benson’s syndrome or posterior cortical atrophy could be regarded as the opposite of developmental synaesthesia associated with special abilities in visual perception such as super-recognition ability and exceptional reading ability, a cluster of traits that appears to run in at least one family. Got that? The point I’m trying to make is that I published this stuff in June 2012, I thought of these ideas independently and as far as I can tell no one else had previously published these ideas anywhere, including in scientific journals.

Now take a look at this paper in a neuroscience journal which was published in 2013 and was received by the journal as a draft or manuscript on July 31st 2013:  http://journal.frontiersin.org/Journal/10.3389/fnhum.2013.00563/full

Do any of the themes in the paper seem familiar? Does my blog or myself receive any credit or acknowledgement in the paper? Hmm.

Regardless of any issues related to originality or acknowledgement, the important point in all of this is that here we have some ideas about a type of dementia which could conceivably have some medical or scientific use or value. My idea of linking synaesthesia with the immune system is nice but just a step in a possibly much more important sequence of ideas. I’d like to give those ideas another airing, while also restating that I thought of them a long time ago independently and claim all due credit. I hope you don’t mind.

There’s a back-story to my theory

I can show data dating back to the year 2000 that supports my theory that low levels of complement proteins, which are a part of the human immune system, specifically C3, C4 and most likely C1q, are the biological cause of the development of inherited synaesthesia (at least in some cases). Before I had thought of the idea of a link between the immune system and synaesthesia I had, at the blog, published a theory that synaesthesia is in some way the neurological opposite of a variety of dementia named Benson’s syndrome (aka PCA, posterior cortical atrophy), based on my observations and reading. I had speculated that there could be some “magical chemical” that regulated the brain in some way and that oppositely extreme levels of this magical chemical could be the biological basis of both synaesthesia and Benson’s syndrome. Back in 2012 I read a small article in New Scientist magazine that blew my mind, because it appeared that it gave me some major clues about what that magical chemical could be. The article was about the exciting work of Dr Beth Stevens on microglial pruning in the brain and the immune system’s complement proteins. The term “pruning” was familiar to me from all of my reading about synaesthesia, which is a fun heritable brain-based phenomenon which I share with some of my first-degree relatives, along with specific gifts in literacy skills. The term “complement” in the context of the immune system, and the individual names of complement proteins were also familiar to me.

Being a super-recognizer, I’m pretty good at recognizing patterns, and I recognized that all these elements of information fitted together into an important and original multi-faceted theory. I was so excited that I published a brief outline of my theory at this blog in 2012. In 2013 I was shocked to discover that a prominent synaesthesia researcher and her co-author had published a theoretical journal paper titled “The immune hypothesis of synesthesia” which even included speculation that the “complement system” could be the element of the immune system responsible for the development of synaesthesia. I found no credit given in that paper to me or my blog. As I had published my theory first I believe I should have been fully acknowledged. I never thought that this could have been a case of two separate parties thinking of the same idea independently. I read their paper through and I looked into the educational and research background of both authors and their previous publications and found no study or writing about the immune system and no indication or explanation of why they might have suddenly had their own insight linking synaesthesia with some of the many elements of the incredibly complex immune system that only an immunologist would find interesting. 

This Easter I’d like to pose the question; can Simner and Carmichael offer data dating back to the year 2000 as the basis of their published version of “the immune hypothesis of synesthesia”? I can, and I would be willing to share my data with serious medical researchers.

A while ago I was sorting through some piles of old papers that I had stowed away years ago without sorting through them. These things happen during a busy family life. These piles had been sitting around for years, some of it photocopies of articles from New Scientist magazine that had struck me as interesting but which I hadn’t always had the time to read through properly. I was amused to find that I had stowed away an article from the March 1st 2008 issue titled “Thought control” by Bijal Trivedi. It was all about exciting research by the likes of Carla Shatz, Ben Barres, Simon John, Staffan Cullheim, Eliezer Masliah, Robert Terry and Lisa Boulanger about synapse loss in dementia and the interesting things that elements of the immune system appeared to be doing in the brain, contrary to the received wisdom that there is a thing called the blood-brain barrier that keeps the immune system out of the brain. I’m not sure whether or not I had read the article back then, but I can understand why it had sparked my interest. Back then it wasn’t enough of a spark to give me the idea of a link between the immune system and synaesthesia, because back then I hadn’t even heard of the terms “super-recognizer” or “Benson’s syndrome”, in fact the concept and the term of “super-recognizer” hadn’t yet been published. Back then I had not the slightest inkling that I had better than average ability in face recognition, so I hadn’t started thinking about whether it was more than a coincidence that I was both a synaesthete and a super, and which parts of the brain might be atypical in both. I hadn’t read the human interest story in The West about a Perth citizen who had been diagnosed with Benson’s, and felt curious about how the description of that type of dementia sounded like the opposite of skills that were superior or associated with synaesthesia in myself and kin. I must have forgotten about the content of the 2008 New Scientist article, if I had ever read it at all, because it would have been the ribbon which I could have used to wrap up my package of ideas neatly. Curiosity can be rewarded, even if it takes a couple of coins before the penny drops.

 

Thank you PubPeer

Thank you PubPeer for (after some fussing about) giving me a place on the internet that is recognized by scientists to publish my objection to some researchers publishing a highly original idea that I had thought of independently and had published at this blog over a year before their draft paper was received by their publisher. I’m certain that this is a case of plagiarism, but other people object to my use of that word, so the only place you will see the word plagiarism used in relation to that matter is here at this blog.

I have already published a very full account of my side of the story at this blog, but unfortunately this blog isn’t recognized as a part of the ecosystem of commentators attached to the world of science, the people and organizations in the league of science journalists, science magazine bloggers and internet services that are supposed to review the science literature but actually appear to be automatically-generated content. PubPeer isn’t like that; it appears to be run by people, but who they are is a mystery. I can completely understand why they wish to remain anonymous. Exposing the many ways in which peer review in science publishing is broken is a pastime that I am sure could be harmful to one’s career in science.

I believe that I can make a greater contribution to science as a blogger who has no job that is in any way connected to any university or any research institution, because I don’t have to deal with career-building and politics that goes with having that kind of career, and as a result I have more “mental bandwidth” free to devote to thinking about actual science. I am not expected to teach half-interested university students or organize conferences or write full-sized published papers or book chapters, and I’m not expected to know my proper place in the scheme of things. Very ordinary physical activities that I do in my everyday domesticated life automatically activate regions of my brain that deal with conceptual thinking and memory, and as a result I am often bombarded by novel ideas resulting from a boundless miscellany of concepts flashing onto the centre stage of my mind and colliding in a quite haphazard manner. I guarantee this kind of involuntary mental activity wouldn’t happen if I spent my days comfortably sedentary inside an airless office, staring at a wall or a dusty old painting. I’ve had jobs like that in the past, and years of study at an austere and ugly university which was also pretty much the staring at a wall lifestyle. I find it ironic that study at a university can offer an environment that has an effect on thought that must surely compare with a lobotomy.

Being a nobody to the world of science has many up-sides. I don’t feel a lot of need to consciously or unconsciously self-censor my ideas and publications to fit in with the beliefs and fashions of researcher peers (whether they make sense or not), and I don’t limit my thoughts to my job description, because I have no job description (and I also unfortunately have no salary, pay or financial benefit of any kind). Having no identity in the world of science means I also have no specialization or niche, leaving me free to see and write about a completely obvious connection between synaesthesia, an area of science typically researched by research psychologists and non-clinical neuroscience/psychiatry researchers, and the human immune system, an area of science that has I guess typically been researched by practicing medical doctors in the specialties of immunology or rheumatology. For sure there have been in the last ten years or so a group of pioneering and original researchers who have researched the incredibly complex ways in which the human immune system impacts on brain development, but I don’t think any of them have linked their work with synaesthesia or any particular type of dementia, as I have.  I’m guessing that they haven’t written about synaesthesia because they feel that it is too trivial a matter for them to bother with, which is probably a defensible point of view, as synaesthesia isn’t a disorder and I’ve never heard of a synaesthete who is looking for a cure. I feel free to write about concepts such as dementia, the complement immune chemicals and synaesthesia that are areas that are beyond my expertise, because I have no recognized area of scientific expertise or any recognized career in science. A lot of words have been written about the concept of intellectual freedom in academia, but I have found that being a non-entity outside of all that is a state that offers the most intellectual freedom. It’s a bit like being the invisible man; you can get up to all kinds of stuff but you can’t hope for recognition, because you have no face and no identity.

Being nobody is a state of freedom but it certainly has it’s frustrations, like having no income as reward for any of the work I put into this blog and the ideas published in it, and having no recognition, not even on the internet, but the most frustrating thing is the way that my most important idea has had no apparent impact in science. I’m not referring to my idea linking the immune system with synaesthesia, which was just an amusing step in my journey to the much more important idea that one particular type of dementia, known by the names Benson’s syndrome or posterior cortical atrophy or PCA, could be caused by an excess of one or more of the complement immune chemicals. Surely this is an idea that could be researched. Surely this is an idea that could lead to a number of different ideas for therapies if it turns out to have some value. Surely this is an idea worth at least checking, for if it reflects reality it surely has the potential to save minds and brains and lives. HELLO! Is anybody listening?

P.S. Late last month an Australian biotechnology company plunged on the stock market following the announcement of the failure of their drug aimed at treating Alzheimer’s dementia during a stage of a study. After years of hoopla and hype about drug companies finding a cure for Alzheimer’s or dementia, and anyone’s guess how much money spent on studies, all they can offer is symptomatic treatments. The story has been one failure after another. Benson’s syndrome is considered by some to be a variant of Alzheimer’s disease. Whether it is or not, maybe it is high time for researchers to stop obsessing about plaques in the brain and look at the immune system and the brain. My money is on C3 and C4 as concepts to focus on in a search for an understanding and cure for dementia. Would it kill you dementia researchers to accept some advice from a Perth blogger who is nobody in particular, and put my name on your research paper if my idea works out?

Some ideas that I’d like to (explicitly) lay claim to (right now) in 2014

A note of warning – If you are thinking about copying or plagiarizing any of the text, ideas or descriptions in this post or using it in your own work without giving me (C. Wright, author of the blog “Am I a Super-recognizer?”) the proper acknowledgement and citations, then think again. If you do that you will be found out and my objection will be well publicized. If you believe that you published any of these ideas before I did, please let me know the details in a comment on this article. If you want to make reference to this blog post or any of the ideas in it make sure that you state in your work exactly where you first read about these ideas. If you wish to quote any text from this post be sure to cite this post at this blog properly. There are many established citation methods. If you quote or make reference to material in this blog in your work, it would be a common courtesy to let me know about your work (I’m interested!) in a comment on any of the posts in this blog. Thank you.

The idea that Benson’s syndrome or posterior cortical atrophy or PCA, a variety of dementia, is caused or develops in a way that can be seen as the opposite of the synaesthesia linked with exceptional visual memory and literacy skills that runs in my family (this idea has been explored previously in this blog).

The idea that the above cited states develop or are caused in a way that makes them seem like opposites because they both affect the same or similar areas of the brain, but in opposite ways.

The idea that the above described process happens because Benson’s syndrome and our variety of synaesthesia are both mediated by the same or similar natural chemical or cells or biological agent in the brain, one caused by high levels of the mystery substance and the other caused by low levels (a hypothesis that I briefly suggested in January 2011).

The idea that one of the many known or unknown elements of the immune system that impact brain development is the mystery substance referred to above (a hypothesis that I briefly outlined in 2012).

The (implied in above ideas) idea of the immune hypothesis of synaesthesia. (This idea was first published by me in 2012 in a blog post archived here, was I believe plagiarized in 2013 here, and was the subject of my plagiarism claim here.)

The idea that one or more of the complement immune chemicals is the  mystery substance referred to above.

The idea that the C3 complement immune chemical  is the  mystery substance referred to above.

The idea that synaesthesia is linked with one or maybe more immune diseases or conditions caused by low levels of complement.

The idea that genes for synaesthesia stay quite common in the gene pool because of some associated cognitive advantage (probably superior memory) that balances out any disadvantages caused by deficiencies in the immune system.

The idea that some or many people unintentionally experience a memory process that operates in a similar way to the method of loci memory technique in their everyday lives, unintentionally forming long-term associations between individual learned concepts and individual visual memories of scenes (I have named this phenomenon Involuntary Method of Loci Memorization or IMLM).

The idea that IMLM operates in such a similar way to synaesthesia that one could argue that it is a type of synaesthesia.

The idea that synaesthetes are more likely to experience IMLM than non-synaesthetes.

The (implied) idea that the method of loci memory technique is similar to or a type of synaesthesia.

The idea that synaesthetes might have a natural advantage in using the method of loci because the method of loci is similar to or is a type of  synaesthesia. This idea that seems likely in light of the case of “S” the Russian memory performer with many types of synaesthesia described by Luria. 

The idea that IMLM is a phenomenon that is caused by enhanced synaptic plasticity throughout the life span.

The idea that IMLM is a phenomenon that is caused by enhanced synaptic plasticity throughout the life span and can thus be used as an indicator of which synaesthetes are synaesthetes due to enhanced synaptic plasticity throughout the life span rather than other possible causes of synaesthesia. Support for this idea comes from the fact that IMLM appears to be a non-developmental variety of synaesthesia that can form new long-term associations in adolescence and adulthood.

The idea that IMLM is a phenomenon that is caused by the unusual possession of levels of synaptic plasticity typical of a young child, during adolescence or adulthood.

The idea that IMLM is caused or enhanced by some characteristic of the immune system that affects the functioning of the brain. Many different elements of the incredibly complex immune system are thought to affect the functioning or development of the brain, and could thus be involved in IMLM, including the complement system, microglia and the MHC class I molecules. Researchers such as Beth Stevens and Carla Shatz have investigated this exciting area of neuroscience. In 2012 I hypothesized at this blog that synaesthesia could be caused by low levels of complement, this idea implying that the immune system is directly involved in synaesthesia (or at least some cases of synaesthesia). I believe these ideas were plagiarized in a paper published in 2013.

The idea that IMLM is similar to the “Proust phenomenon” in that it is very similar to synaesthesia or is a type of synaesthesia and involves episodic or autobiographical memory as a concurrent.

The idea that phonics as a foundational reading skill is similar to or is arguably a type of synaesthesia in that it involves the involuntary association of individual speech sounds with individual printed letters or combinations of letters, as the result of learning in early to mid childhood.

The idea that at least one type of dyslexia is like a deficiency of synaesthesia.

The implied idea that if synaesthesia has as it’s basis hyperconnectivity in the white matter of the brain, dyslexia as an opposite of synaesthesia or a deficiency of synaesthesia is or could be caused by hypoconnectivity in the white matter of the brain (I suspect there might be existing research evidence that supports this idea).

The implied idea that in at least one cluster or grouping of cases synaesthesia is associated with superiority in literacy or reading skill.

The idea that synaesthesia can happen in different regions of the brain, and because of this the experience of various types of synaesthesia can vary in detectable ways because of the influence on the synaesthesia of the varied ways that different areas of the brain operate. This can mean that one synaesthete can experience different types of synaesthesia that operate in very different ways, for example, some types of synaesthesia more rare or spontaneous or intrusive than other types. (I am not completely sure of the originality or the novelty of all of this idea.)

The idea that there is an association between synaesthesia and super-recognition that is not merely coincidental.

The idea that synaesthesia is a type of memory or learning. (Not sure if I’m the first to note this obvious fact).

The idea that synaesthesia concurrents are re-experienced memories, or re-activated “learnings” of concepts, not perceptions. (Not sure if I’m the first to note this obvious fact). In support of this idea I can assert that synaesthesia is like face recognition in that both are visual memory-based phenomena which are subject to the Verbal Overshadowing Effect or something very similar. My assertion that synaesthesia is subject to the verbal overshadowing effect is based on my own observations (outlined elsewhere in this post).

The idea that super-recognizers should or could be trained and employed as expert consultants in the practice of medical genetics.

The idea that medical geneticists and all types of medical specialists need to have a super-recognizer level of face memory or face recognition ability, so that they can intuitively and quickly recognize medical facies.

The idea that there is no clear point of distinction between medical facies or faces associated with genetic syndromes and normal faces.

The idea that super-recognizers could be used to facially identify blood relatives of a person or persons.

The idea that super-recognizers could be used to facially identify the specific ethnicity of a person.

(below ideas added January 28th 2014)

The idea that super-recognition or being a super-recognizer could develop as the result of an unusual level of fascination with the visual appearance of landscapes or scenes, rather than from a fascination with faces, and thus be a side-effect hyper-development of a part of the brain that serves two similar functions.

The idea that super-recognition or being a super-recognizer could, at least  in some cases, develop as the result of a general hyper-development of the visual sense to compensate for problems in the auditory sense during childhood such as temporary deafness, recurrent ear infections, glue ear or poor auditory processing.

(below idea added February 1st 2014)

The idea that lexical-gustatory synaesthesia is an exaggerated form of some kind of evolutionary adaptation in the brain that biologically primes the mind to attend to or react to speech on the subject of food (this idea was discussed at this blog in a post dated January 27th 2011, with more consideration in a later post).

(below ideas added February 6th 2014)

The idea that creativity might be immediately enhanced during and only during the duration of physical or visual-spatial activity because the activity activates areas of the brain associated with movement and in turn these areas activate other areas of the brain including those that give rise to conceptual thinking, and the increased activation makes novel associations between diverse thoughts and concepts more likely, and that this process is like synaesthesia or is a type of synaesthesia, and the types of physical activity that are the most effective inducers of this effect might be highly specific, highly specific in effects, highly varied between individuals and highly idiosyncratic, as is typical of synaesthesia inducers and concurrents. Driving a car can act as an inducer of this effect. (I have gone some way to exploring this idea in past posts.)

The idea that mental flexibility might be immediately enhanced by the above effect, which I will name “movement – thought-flexibility synaesthesia”.

The idea that thinking might be immediately enhanced by the above effect.

The idea that memory might be immediately enhanced by the above effect.

The idea that the above effect is similar to embodied cognition or is a type of embodied cognition.

(below ideas added February 14th  and  February 20th 2014)

The idea that synaesthesia is like the process of face recognition (and vice versa), because they both

– are subject to the verbal overshadowing effect or something similar

– are automatic

– are involuntary

– have a sensory inducer, in face recognition always visual, in synaesthesia I think most frequently visual

– have or can have a concurrent that could be described as a memory, a concept or a personality (I’m comparing face recognition with personification synaesthesias and the synaesthesias that I have described at this blog which have visual memories of scenes as concurrents)

– are or can be visual in both the inducer and concurrent

– typically involve the fusiform gyrus

– involve set pairings of inducers and concurrents (same person’s face seen before then recognized later)

– involve set parings of highly specific inducers and concurrents (I recognize that an employee at my local supermarket has a sister who has just started working there too, as their faces and bodies and hair are near-identical, but for the extra acne and the more receding chin of the new employee. They are very similar in appearance but my discrimination is highly specific, just as I can recognize that the green wall on the lower floor of a public library is close to but not quite the same colour as Tuesday.)

– both can have, but do not always have an actual face as an inducer (we can recognize the faces of celebrities in photos, caricatures and art, even seeing Marilyn Monroe’s face in a pattern of brown coffee cups stuck to the wall at the coffee shop at the art gallery.)

(below idea added February 17th 2014)

“My particular interest in personification is my own theory that personification synaesthesia (as experienced by myself) or something like it gives rise to superiority in face memory (or being a super-recognizer) by naturally making the faces of unknown people more memorable and interesting”

The above is a quote from an article that was published at the blog in October 2013.

(below ideas added February 19th 2014)

The idea that the synaesthesia brain is the result of the developmental influence or shaping from, or the adaptation to, the behavioural phenomenon of “flow” as described by Mihaly Csikszentmihalyi.

The idea that synaesthesia, intellectual giftedness or high IQ and autism or Asperger syndrome seem to coincide more often than chance because gifted and autistic kids are more likely to experience “flow” and this in turn can influence the developing brain in a way that gives rise to synaesthesia.

(below ideas added February 20th 2014)

The idea that the genuine conscious awareness of synaesthesia is a threshold phenomenon that operates in conflict or competition with conscious thinking, meaning that consciously thinking about synaesthesia can inferfere with the perception of concurrents, and synaesthesia must reach a particular level of intensity before it interrupts the experience of consciousness and becomes itself the subject of conscious awareness. I think that the idea that thinking about synaesthesia can interfere with the perception of synaesthesia might be related to the “verbal overshadowing” effect which has been described and debated about by researchers. In fairness I should point out that Mark C. Price speculated in the recently published (2013) Oxford Handbook of Synesthesia that synaesthesia could be subject to the verbal overshadowing effect. My own ideas were arrived upon independently from Price’s writing or work.  I base the ideas of synaesthesia being a threshold phenomenon which can also be interfered with by conscious thinking on a number of my own observations. In direct contradiction to what I had expected to find, my scores for accuracy for individual letters and numbers in The Synesthesia Battery (a scientifically-validated online test of synaesthesia) were lower for the numbers and letters that have colours that I find beautiful and which I have thought about to some degree, while my best accuracy was for the numbers and letters that have the dull and ugly colours. It seems the less I think about the concurrents the more accurately I can percieve them when they are evoked. I have also noticed that most of the types of synaesthesia that I experience I was not consciously aware of before I started to think about and examine the idea of synaesthesia. I never realised that I had complete stability in the colours I associate with months and days of the week till I tested myself. While I had a dim awareness of colour colouring my thoughts, I’d not realised that this worked like synaesthesia till I went looking for a pattern using simple testing. My fine motor movement-visual memories of scenes synaesthesia evokes concurrents that are so fleetingly and subtly experienced that they just feel like random thoughts, and indeed I now believe it is possible that the random thoughts of many or even all people are in fact synaesthesia of various types. I have also observed that there are some very unsubtle and intrusive types of syn that I experience, and they are typically rarely experienced and are associated with people, emotions, faces, singing voices or music that I find striking or novel as inducers. Because of the circumstances of these examples of synaesthesia, I think some kind of threshold is being breached when these types of synaesthesia are experienced by me.

The idea that one of the established defining criteria for synaesthesia, that it gives rise to perceptions or concurrents which are “consistent and generic (i.e., simple rather than pictorial)”, is wrong, and specific categories of memories of complex visual images such as faces and scenes, which are processed in the fusiform gyrus, can also be experienced as genuine synaesthesia concurrents. I base this assertion on the fact that I often involuntarily experience synesthesia concurrents of this type, and I have written about such experiences right from the first post in this blog which was published in 2010. I have also named types of synesthesia that have complex visual memories as concurrents: the strange phenomenon, fine motor task – visual place memory synaesthesia, involuntary method of loci memorization, etc. There are also many accounts or scientific observations of synaesthesia with complex visual concurrents in the scientific literature on synaesthesia.

Have my ideas been plagiarized in a paper published in a neuroscience journal? I believe they have.

This post replaces a brief temporary posting which was previously published here, with the notice that it would be added to at a later date when I had more time. I’m a busy parent who gets paid nothing to write and I have struggled to find the time to give this important matter proper attention. Do not be surprised if you find this post edited or altered.

I’ll get to the point straight away. I believe that I am the victim of plagiarism. At the very least, I believe that I have scientific priority in regard to a group of related scientific ideas or hypotheses, and my priority in regard to two of those ideas has not been recognized, and as a result some ideas which I published at my blog in 2012 have been presented in a journal paper that was published this year as though those ideas were new. The two ideas which were re-published by others in 2013 as though they were their original ideas are the idea that synaesthesia could be caused by unusually low levels of complement (a group of immune system chemicals) and also the idea implied by that idea that synaesthesia could have as its origin some peculiarity in an element of the immune system which plays a dual role in the development of the brain. The complement chemicals are certainly not the only elements of the immune system which are thought to influence the brain. I am not alleging that plagiarism in the form of word-for-word copying of text has happened in regard to the documents cited below. I am alleging that plagiarism of ideas has happened, and even though this type of plagiarism is not easy to prove, I can prove that I published my blog article introducing my ideas over a year before the journal  paper by the others was even received as a manuscript by the journal which would eventually publish it.

Below are the details of my blog post published in June 2012 which contains the ideas which I believe have been plagiarized:

Wright, C. Is synaesthesia caused by low levels of complement? Is Benson’s syndrome (PCA) caused by too much complement C3? Could synesthesia and posterior cortical atrophy be considered in some way opposites? Am I a super-recognizer? June 7, 2012.

https://superrecognizer.wordpress.com/2012/06/07/is-synaesthesia-caused-by-low-levels-of-complement-is-bensons-syndrome-caused-by-too-much-complement-c3/

and permanently archived by the Internet Archive Wayback Machine on June 21st 2012: http://web.archive.org/web/20120621071430/https://superrecognizer.wordpress.com/

Below are the details of the published journal paper which includes what I believe is plagiarism of my ideas, or at the very least the re-publication of my ideas without any acknowledgement of me or my writing:

Carmichael, Duncan A. and Simner, Julia The immune hypothesis of synesthesia. Frontiers in Human Neuroscience. 2013; 7: 563.

Published online 2013 September 11. doi:  10.3389/fnhum.2013.00563

Received July 31, 2013; Accepted August 23, 2013.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769635/?report=classic

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769635/    (see the “article notes” at this version to view all the dates relevant to publication of this paper.)

http://www.frontiersin.org/human_neuroscience/10.3389/fnhum.2013.00563/full

https://pubpeer.com/publications/13259457EAEBF97186167E7BDFB6B3

Please note the dates cited relating to the process of getting this paper published. There is nothing in those dates that could serve as evidence that these authors independently thought of the ideas in the paper before I published my blog piece. I published my blog piece in June 2012 and the above paper was received by the above journal in July 2013. The authors could have been wildly plagiarizing during the thirteen months or so after I published my piece and before their paper reached the offices of the journal.

I think it is important to point out that I had no contact or communication with either of the authors of the above journal paper about my ideas about synaesthesia and the immune system during the period before their paper was published. I did not inform them about or discuss my ideas on this subject privately and I did not privately grant them permission to use or publish my ideas, and I am not one of the “anonymous reviewers” who made “helpful comments” on the manuscript of the above paper, who were mentioned in the acknowledgements section of the above paper. Shortly before I published my ideas about synaesthesia and the immune system I did have a short and one-sided email correspondence about some of my ideas with a microglia researcher and I also sent a non-specific email off to a local medical specialist. The authors of the above journal paper did not privately inform me about any ideas or theories linking the immune system with synaesthesia before the publication of my blog post on that subject. It is my sincere belief that my ideas in that post were new and original and had not previously been published. I also did not receive any information or “leaks” about the work of the authors of the journal paper from any third party.

If you take a careful look at the details of my blog post you might notice that one of my scientific hypotheses is presented within the internet address of that posting and also within the title of the posting, and the internet address also contains details of the date of publication. Like all of the internet addresses of the posts at this blog, it was automatically generated by WordPress when I published the post. The date of publication is also automatically added to the blog post during publication, as is the name of the author. Unfortunately, the date of blog posts can be altered post-publication, with this alteration reflected in the web address of the post and the situation of the post in the chronological sequence of the blog. While the blog can be altered, one cannot alter blog readers’ memories of my blog posts and any records that they might have kept of them, and this blog has a diverse and steady readership. In situations demanding proof of the date and also the content of a document published on the internet, one free resource on the internet is invaluable; the Internet Archive Wayback Machine. This internet archiving service archived my June 7th 2012 blog article on two different dates in two different forms. The earlier archived record was recorded on June the 21st 2012 with the blog post included in a record of the whole home page of my blog on that date.

http://web.archive.org/web/20120621071430/https://superrecognizer.wordpress.com/

This date was only a fortnight after the post was first published and over a year and a month before the others’ journal paper was received as a manuscript by the journal that would later publish it. This proves that my blog post was published on the internet at least before June 21st 2012, a long time before the journal paper was published online or in hardcopy, or was even received by the journal publisher. The content of my blog post as was published then is also documented and can be checked. The blog post was also archived in November 2013 within an archive of a month’s blog posts.

In addition to citing the archived old record of my blog post as evidence, there is other evidence that I can cite to show a long history of me expressing ideas such as those in my blog post, ideas that overlap with ideas presented in the journal paper, and many more novel, original and inter-related ideas besides. The origin and development of the ideas in my blog piece can be traced back a long way in time within my own writing at my blog. I theorized not only that synaesthesia could be caused by low levels of the immune chemical complement, I also theorized that a form of dementia, which to my knowledge has never by anyone else been linked to or contrasted with synaesthesia in scientific discussion, could be caused by excessively high levels of complement. I also theorized that this type of dementia, Benson’s syndrome or PCA, could be seen as the opposite of synaesthesia or at least the opposite of the cluster of unusual functional characteristics of my own brain. Implied within this theory is the idea that there is some kind of network within the brain of parts that are especially sensitive to some factor that influences growth or pruning or cell death, because the same mental functions appear to be boosted at least since early childhood in the brains of me and some of my first-degree relatives which decline in Benson’s syndrome. I have no reason to believe that the early specific cognitive enhancements are some unknown facet of Benson’s, because there is no particular history of dementia in my family. I still see the two conditions as opposites, potentially with one common factor (extreme levels of some influential chemical) unlocking the mystery of both. My post published in June 2102 was not the first place where I published my own ideas about Benson’s syndrome being the opposite of synaesthesia. I had first written about this apparently original and new idea in a blog post published in January 2011:

https://superrecognizer.wordpress.com/2011/01/04/the-opposite-of-bensons-syndrome/

This blog article was archived and recorded by the Internet Archive Wayback Machine in March of 2011:

http://web.archive.org/web/20120308215442/https://superrecognizer.wordpress.com/2011/01/04/the-opposite-of-bensons-syndrome/

It is clear that my ideas in my June 2012 blog post were a development of ideas that I had already published at this blog in January 2011, indeed I quoted from my earlier blog post in my latter blog post. My earlier blog post has been archived by a third party and stands with other related blog posts as a record of the direction and date of the development of my ideas, which are very congruent with the many ideas expressed in my June 2012 blog post. In contrast, it appears to me that that the authors of the journal paper which I believe is a plagiarism of ideas in my blog post cannot demonstrate any published and/or archived set of documents that show the development of their ideas towards any theory linking synaesthesia with any element of the immune system. I believe this because I have done a quick check of the lists of past publications of both authors. I have not been able to trace any development of theories about synaesthesia in their work or academic collaboration that might lead them to look at the immune system, and I was not able to find any hint or explanation in the journal paper itself about why these researchers arrived at a theory about the immune system. In my opinion, their theory linking synaesthesia with the immune system appeared “out of the blue” within the context of their own published research and published papers. If anyone can identify any dateable and/or archived document by either of the authors of the journal paper that shows an early development of the idea of linking synaesthesia with the immune system then I would be very interested to see that document, and I request that a comment detailing such document be left at this blog. The apparent absence of evidence of a theoretical progression or development towards “the immune hypothesis of synaesthesia” in the published work of the two authors of the journal paper is one reason why I cannot believe that they conceived of the immune hypothesis of synaesthesia independently as a team or as individuals.

The immune hypothesis of synaesthesia would not have been proposed had it not been for the work of researchers who investigate the dual roles of elements of the immune system which also play a role in brain development and neuroplasticity. The authors of the journal paper have primarily cited the work of Assistant Professor Lisa Boulanger who studies MHC Class 1 proteins, while in my blog post I concentrated on the work of Assistant Professor Beth Stevens who studies microglia and complement. It appears to me as though the authors of the journal paper have made a deliberate decision to anchor their theoretical ideas onto a different existing body of research in molecular biology than the body of research that inspired my theories. I believe they had the aim of distancing or differentiating the content of their paper from the content of my blog post. I first learned about the work of Beth Stevens from reading a June 2012 article in New Scientist magazine. Although the authors of the journal paper evidently at some point in time developed an interest in the work of Boulanger and consulted her during the writing of the paper, it is not clear why in 2013 they should be publishing a paper at least in part inspired by her work, because the papers of hers cited were published in the years 2004, 2009 and 2010, hardly the latest news in neuroscience. The most recent items in the journal paper’s references list relating to the immune system and the brain are a 2012 paper by Elmer and McAllister and a 2012 paper by Beth Stevens and two other authors. Boulanger does molecular biology at Princeton University in the United States while the authors of the journal paper do psychology and psychiatry at Edinburgh University in the UK, so it seems unlikely that the three by chance swapped ideas over lunch.

I have noticed an absence of mention of or enthusiasm for the immune hypothesis of synaesthesia in 2012 and 2013 media coverage and conference presentations featuring either of the authors of the journal paper, and I find this curious. It appears that they deliberately kept quiet about the hypothesis before it made it into publication. Why?

One of the authors, Duncan Carmichael, was interviewed for the British radio show The Naked Scientists on October 7th 2012, and his research on synaesthesia was the subject of the discussion:

http://www.thenakedscientists.com/HTML/content/interviews/interview/2269/

Even though this interview was conducted roughly nine months before Carmichael’s and Simner’s journal paper about synaesthesia was received by the journal as a manuscript, no evidence of a conception of the idea of an immune hypothesis of synaesthesia can be found within Carmichael’s answers in this interview. He spoke about a genetic study, but said not a thing about the immune system. I find it hard to believe that a researcher who gave such an ordinary account of the contemporary state of knowledge and research on synaesthesia was a member of the team who generated one of the most original ideas in synaesthesia research for a long time. Wouldn’t he have been barely able to contain his excitement about the novel scientific theory? I know that is how I felt about it when I thought of it.

This is a university web page outlining the work of Duncan Carmichael:

http://www.anc.ed.ac.uk/dtc/index.php?option=com_people&func=showall&userid=387

I cannot find evidence of a lot of originality in thinking or the development of ideas about the immune system in the work detailed at this page. It looks like some standard ideas about synaesthesia explored by a PhD student whose background in psychology and psychiatry is pretty standard for synaesthesia researchers.

An abstract of a conference presentation delivered and co-authored by Duncan Carmichael can be found at the below link and a link to what appears to be the slide images used in that talk can also be accessed at the below link:

http://www.synesthesia.info/recent.html

This conference was the Tenth Annual National Conference of the American Synesthesia Association held in Canada May 31 through June 2, 2013, roughly two months before the immune hypothesis of synaesthesia paper was received by the journal as a manuscript. I looked at the abstract and also the slide show and I found a spelling error and some questionable unexplained assumptions in the slide presentation but I found no hint of the development of the immune hypothesis of synaesthesia. I find it remarkable that Carmichael could have co-written and submitted a publishable a paper containing some highly original and paradigm-shifting ideas barely a couple of months after giving talks at a conference about the same general area of research which gave no clue about the intellectual development of the novel ideas. When I look at the highly conventional and ideas about synaesthesia in Carmichael’s written work, media appearance and May-June 2013 conference presentation I find it impossible to believe that he is a part of the team that theoretically wed synaesthesia with the immune system for the first time based on their own ideas. One could argue that Carmichael was deliberately keeping the new theory a secret, but what can account for the contrast between the conventionality of his other work and the originality of the immune theory?

Perhaps the originality of the novel idea was the contribution of the other author? I’ll happily admit that Dr Julia Simner’s work on synaesthesia has consistently been interesting and she has made important and fairly novel contributions, but I could likewise find nothing in her work or in her academic background to indicate a curiosity about or knowledge of the immune system. Dr Simner categorizes herself as a cognitive neuropsychologist, and her academic background is in “psychology, languages and linguistics”.

This is a link to her university web page in which Carmichael is listed as a student supervised by Simner:

http://www.ppls.ed.ac.uk/people/julia-simner

Two 2013 media appearances are listed at the above page. One was at the Guardian Edinburgh International Television Festival. These are pages related to an August 2013 talk by Dr Simner at that festival:

http://www.audionetwork.com/content/whats-new/events/geitf/julia-simner-q-and-a

http://www.audionetwork.com/blog/author/dr-julia-simner/2013/8/27/synaesthesia—a-merging-of-the-senses.aspx

http://www.audionetwork.com/show-article.aspx?id=386

Unfortunately a recording of that talk appears to be no longer available. The talk was presented while the immune theory paper was in the process of being published but I found no hint of the paper’s theme in the page about Dr Simner’s talk.

This is the page about an appearance that Dr Simner made at the Edinburgh International Science Festival on April 1st 2013:

http://www.sciencefestival.co.uk/whats-on/categories/activity/sensory-dining-1404

A PDF of the festival’s 2013 programme can be accessed here:

http://www.sciencefestival.co.uk/uploads/EventImages2013/Edinburgh%20Science%20Festival%202013%20brochure.pdf

There’s nothing related to the immune system to be found in info about that appearance.

A Word document of Dr Simner’s CV can be downloaded from Simner’s university page:

http://www.psy.ed.ac.uk/people/view.php?name=julia-simner

Simner’s CV includes a quite up-to-date list of the publications. I searched her CV and found only one mention of any word that I can think of that is related to the immune system, and it was in the title of the paper under dispute. I couldn’t even find one example of use of the words “synapse”, “synaptic”, “plasticity”, “pruning” or “neuronal” in Simner’s CV, which I take as an indication that Simner’s research on synaesthesia could hardly be described as “biomedical”, except for that one paper which stands out like dog’s balls within the contexts of the other work by Simner and by Carmichael. I invite you to check for yourself and let me know if I have missed something.

Here are some other links to information about Dr Simner:

http://www.biomedexperts.com/Profile.bme/1310901/Julia_Simner

http://www.research.ed.ac.uk/portal/en/persons/julia-simner(616de62b-07c6-430d-b217-d18880744549).html

http://ukcatalogue.oup.com/product/9780199603329.do

http://community.frontiersin.org/people/u/68706

I have argued that the originality of the immune hypothesis of synaesthesia stands in contrast with the conventionality of Carmichael’s other work and also stands in contrast with the lack of medical or molecular biology focus in Simner’s other work. I could also argue that the originality and the molecular biology of the immune hypothesis stands in contrast with synaesthesia research in general. Stale old models of synaesthesia proposing hyper-connectivity in the brain, inhibition of the process of neuronal pruning or disinhibited or hyper-excitable neurons have been doing the rounds forever. Researchers seem to be satisfied with explaining the biological basis of these theorized neurological peculiarities by suggesting that there are genes for these features, as though that is any explanation at all. The traditional models of synaesthesia seem to owe a lot to a layman’s understanding of simplistic models of psychiatric illnesses and neurodevelopmental disorders (endless guff about neurotransmitters and brain “wiring”) or owe a lot to a superficial resemblance between synaesthesia and hallucinogenic drugged states of mind. There have been genetic studies of synaesthesia and there have been brain scan studies as well, but I don’t think you will find a lot of molecular biology in pre-2013 synaesthesia research.

If the authors of a journal paper read my blog post and took my ideas in that post and used them in their journal paper without acknowledging me, could they have any possible excuse? It is perhaps worth noting that at my blog my name as the author of the posts (my blog is not a collaborative one and only has one author) is not shown on posts at the main page of the blog, but the author’s name in blog posts is displayed when individual posts are selected for viewing, along with any comments about the post. There is no information about me (the author) at the main page of my blog, so I guess it is not inconceivable that a reader might assume my blog is an anonymous publication. Nevertheless, if one wanted to properly cite any of the posts at my blog or the blog itself the title of the blog could be cited. It is a standard practice to cite the first few words in the title of a book or other type of document instead of the author’s name if the author is unknown, and if the author is known to be anonymous they should be cited as “Anonymous”. There is no technical or formal reason why any of the pieces of writing at my blog can’t or could not have been cited.

I can see one possible objection to my claim of having scientific priority regarding the idea of linking synaesthesia with complement and the immune system. It could be argued that my idea was never properly published as my idea, because it was published at a blog and was not published as my idea in a paper or some other document in a scientific journal. Such an objection would be based on the assumption that scientific publication can only happen within a select and specialized type of publication that is widely recognized as a scientific publication, and cannot legitimately be self-published or published in a print publication or internet web site which is not specifically devoted to the publication of scientific research and scientific theories. My answer to this objection is that it is snobbery and it is also at odds with the current realities of our online world. Such an idea seems to be based on the belief that science is an enterprise that legitimately operates like a closed society in which membership is only open to those who have particular credentials or those who have jobs in particular types of institutions (universities or research institutes for example) or those who have the resources and social connections to be able to successfully submit a full-length paper for publication in a peer-reviewed science journal. But the history of science is peppered with examples of scientists who done important work outside of universities, of amateur scientists and gentlemen scientists who have made very important contributions, and of scientists who have offered interesting and respected theories outside of the fields in which they are qualified. There are also plenty of examples of crackpots who present themselves as legitimate scientists and of researchers who have made laughable blunders while straying outside of their areas of specialization. There are also too many examples of scientists who have made serious blunders because they apparently did not know about important and relevant facts or knowledge from areas of science beyond their limited field or from beyond the world of academia. I can also think of some great examples of scientists who have only been able to make important discoveries once they have had the courage to question accepted scientific or medical knowledge. My point is that science is not a neat, closed and orderly enterprise. It can and it should be informed by non-scientists who have specialized expertise and amateur scientists. Science can be seriously failed by academics who are blinkered or who over-reach the limits of their knowledge or who engage in scientific misconduct. If science was a perfect and orderly enterprise we would call it The Church of Science and lecture theatres would be places of worship. Science belongs to everyone; everyone benefits from it and anyone who has good ideas and a respect for evidence can play a part, and should be given due credit.

Even if there were no plagiarism in the journal paper by Simner and Carmichael there are still plenty of things in that paper which I find objectionable. As a synaesthete I am personally offended by the frequent use of negative language in reference to synaesthesia in the paper. Here’s a list of words and phrases from the paper: “neurological condition”, “excess cortical connectivity”, “excess connectivity”, “excessive connectivity is indeed a feature of the synesthetic brain”, “failing to supress non-relevant activation”, “excessive activity of excitatory neurons”, “aberrant connectivity”, and ”misregulated feedback mechanisms”. This repeated use of terminology with negative connotations regarding synaesthesia is certainly not typical of scientific or popular literature on the subject. It is rather amusing when one reflects that these authors are being so negative about the type of mind which I believe provided them with the central idea of their journal paper. Talk about biting the hand that feeds! Even more offensive and stupid is the authors’ described quest to find a link between developmental synaesthesia and the degenerative nervous system disease multiple sclerosis (MS). They aren’t even being as bold as researching a link between diagnosed cases of MS and synaesthesia, they are only looking at “people with the radiological profile of multiple sclerosis”, whatever that means. Developmental synaesthesia is a generally stable inherited neuropsychological variation characterized by white matter in the brain that has been described as having greater volume, greater connectivity or being “more coherent”. It is not considered to be an illness or a disorder, and it appears to be associated with superiority in memory. Multiple sclerosis is an inflammatory disease typically with an onset in adulthood which damages the myelin covers of nerves in the brain and in the spinal cord. While there are some genetic risk factors it is not considered to be a hereditary disease. Vitamin D deficiency and infectious agents have been suggested as causes or triggers. MS causes a wide range of mental and physical problems and disability and substantially reduces life expectancy. It is not known whether is caused by an autoimmune process or a failure of the myelin-producing cells. The only apparent commonality between MS and synaesthesia appears to be that they both feature white matter that differs from the average state, but those differences could be characterized as opposite states, not similar. Simner and Carmichael’s idea that synaesthesia might be more common in those who look like MS cases strikes me as at best bizarre, but apparently they have submitted a paper on this subject. I think I know where that paper might belong.

To offend in so many ways certainly takes some doing, and I do acknowledge that there is a large difference between the amount of effort that went into the writing of my blog post and the amount of work that would have gone into writing and obtaining publication of the journal paper, but I believe that it is also true that the guts of that paper was an idea of mine, and I believe there would have been no paper to work on without my idea.

If I accept the proposition that this apparent case of plagiarism was really a case of two different parties reaching the same conclusion independently and within a year or so of each other, with the others being unaware of the existence of my prior publication, and then they innocently published their own paper as the first to introduce these ideas to the world, then I must ask why they were not aware of the existence of my blog post. Did they think they only had to search the traditional scientific literature to check whether their ideas were truly novel and original? I find that hard to believe, in this online, open-access world. Before I published these ideas at my blog I searched the internet and bibliographic databases to check whether my ideas were really as novel as I thought they were. I found nothing comparable. I am completely sure that my blog post would have been retrieved within the first page of a results display from a simple Google search on the terms “immune” and “synaesthesia” or “synaesthesia” performed in the months and year after I published my blog post. My blog has always done very well in Google searches.

I believe that the immune hypothesis of synaesthesia is the product of a synaesthete brain, my synaesthete brain. If anyone can show evidence that counters this, please let me know by leaving a comment. I have demonstrated that I was the first to publish the immune hypothesis of synaesthesia. I believe that I should have been acknowledged as the creator of this idea by the authors of the journal paper. I’m not pleased with what has happened. I do want my ideas which I have published at my blog to be read, considered and developed by other people. I am not a hoarder of ideas and I’m not out to make trouble. I just want to be contacted, asked and acknowledged, and properly acknowledged in print in the conventional manner if my original ideas are used or referred to in someone else’s work.  I don’t think that is too much to ask.

I don’t see what you see, and vice versa

This blog post from Dr Kevin Mitchell, a synesthesia, brain connectivity and developmental neurogenetics researcher from Trinity College in Dublin at his interesting blog Wiring the Brain is well worth a read, and I think is very relevant to finding an explanation for my gifts and peculiarities in visual perception. I was amazed by the normal variation in size of visual processing areas of the brain, which is probably genetic in origin and isolated from other traits. Australian cognitive science researcher Dr Jon Brock at Macquarie University left a comment suggesting a related possible area for research into autism.

“A negative correlation that has been observed between size of V1 and size of prefrontal cortex in humans might be consistent with such an antagonistic model of cortical patterning.” Fascinating! I’ve got to wonder if this has any relevance to understanding Benson’s syndrome or posterior cortical atrophy or PCA.

Dr Mitchell’s blog has been in my blogroll for a long time, and if you are looking for some interesting holiday reading about the psychology of visual processing or neuroscience, a good starting point might be my blogroll.

Do you see what I see? by Dr Kevin Mitchell December 12th 2012 Wiring the Brain. http://www.wiringthebrain.com/2012/12/do-you-see-what-i-see.html

Don’t forget the parietal lobe – the connections are interesting

If you have been reading this blog for a long time you’d know I’ve been trying to figure out which parts of my brain are responsible for my synaesthesia and related experiences. I’ve found that the right fusiform gyrus is a part of the brain that comes up over and over again, in relation to synaesthesia and also face recognition I experience many types of synaesthesia and also have achieved scores in face recognition tests consistent with being a super-recognizer, so this combination seems significant, and despite a lack of any evidence from other case studies linking synaesthesia with superior ability in face recognition, I still think it is a possible relationship that should be scientifically investigated, especially in light of a pattern of associations which I believe suggests that synaesthesia might be a neuropsychological condition that could be seen as the opposite of Benson’s syndrome, which is a type of dementia that involves a loss of visual perception, apparently including a loss of face recognition ability. While synesthesia is generally an inborn developmental condition, and Benson’s or PCA a neurodegenerative condition with a typical onset late in life, I’ve still got to wonder whether inborn factors contribute towards Benson’s. While Benson’s is considered to be a variant of Alzheimer’s, I don’t think anyone knows why it causes deterioration in different areas of the brain as are affected by Alzheimer’s, apparently the same parts of the brain (at the rear) that appear to be enhanced or hyperactive in my brain, and I also doubt that anyone knows why Benson’s has an onset earlier than Alzheimer’s disease. I’m sceptical of the idea that Benson’s is just Alzheimer’s of the back-end of the brain. I suspect that immune system elements microglia and complement might be central to an explanation for Benson’s syndrome. Reading Dr B. Croisile’s paper about Benson’s I’m struck by the many very strange effects of Benson’s on perception, and I wonder at the ways in which a study of it might inform science about  the workings of the brain. I think it is at least as interesting as synaesthesia, which attracts a lot of attention from researchers. Apparently people with Benson’s cannot imitate movements. Does this mean that the mirror-neuron system which so many neuroscientists have gotten so excited about is located at the rear of the brain? I note that the inferior parietal cortex is one of the parts of the brain that are thought to house mirror neurons.

When I set out to write this post I had actually planned to write about a fairly recent review journal paper focusing on recent research about the most common and well-known types of synaesthesia: coloured hearing, coloured graphemes and time units in space synaesthesia. I really like the paper cited below by Professor Karsten Specht from the University of Bergen in Norway, and I’d recommend it to anyone who wants to learn about the latest knowledge about synaesthesia from just one paper. I only have a couple of gripes about he paper. I wouldn’t describe synaesthesia as “rare” as Specht does. Ward, Sagiv and Butterworth wrote in 2009 that around 12% of the population have number forms, and that estimate doesn’t surprise me. Synaesthesia in general can’t be rare if it includes one type that isn’t rare. Time-space synaesthesia or number forms is one type of synaesthesia which the synaesthete can have but not suspect that it is synesthesia, or anything out of the ordinary, so I’d guess it could be very much under-reported and under-estimated. My other gripe with Professor Specht’s paper is this bit; “In recent years, several studies have attempted to investigate whether synaesthesia is primarily a perceptual or conceptual phenomenon.” I think Specht is here presenting the reader with a false dichotomy. In some of the types of synaesthesia and related phenomena which I experience sensory perception, memory and conceptual thinking are connected with synaesthesthetic linkages, so I doubt that there is much point in trying to characterise synaesthesia as one or another type of phenomenon. I was very excited when I read the book Beyond Human Nature by philosopher Jesse Prinz. Professor Prinz argued that we think in mental images rather than in language. He wrote that “It used to be thought that the back part of the brain is used for perceiving and the front is used for thinking. But we now know that the back part of the brain, where most of the senses are located, is very active when people think. Moreover, we know that the front part of the brain does not work on its own, but rather coordinates and reactivates sensory patterns in the back. Recent evidence from Linda Chao and Alex Martin has shown that reading activates the same areas as looking at pictures, suggesting that we visualize what we read.” In a post that I wrote a while ago I described involuntarily “seeing” in my mind’s eye visual images of landscapes and building interiors from imagination and memory while listening to an autobiographical audio-book. I thought it was probably related to synaesthesia, but it appears that everyone’s brain illustrates text with images when reading. Perhaps synaesthetes do this to a greater degree or in a way that is more available to conscious awareness.

Anyway, back to Specht’s paper. Having read it I now suspect that the parts of my brain that are bigger or better connected or more active or something are: the right fusiform gyrus (including the FFA), the left parietal lobe including the left intraparietal sulcus, the right inferior parietal lobe, the hippocampus (I’m sure is involved with IMLM) and the parahippocampal gyrus. I’d guess that these are the places where interesting things are happening. It appears that the role of the parietal lobe in synaesthesia has been understated in the past. It is now thought that synaesthesia does not solely involve the cross-activation of two different sensory areas (as if it was ever that simple!), but it also requires a “binding” process to happen in the parietal lobe. There is no underestimating the importance of this binding.

If you are as interested in synaesthesia and bits of the brain as I am, you might also like to read a much longer journal paper by Rouw, Scholte and Colizoli that was published last year. It is available in full text at no cost, but I don’t think it covers non-colour types of synaesthesia. Details can be found below. One part of the parietal lobe mentioned in that paper, which is cited by a few studies as involved with synaesthesia is the inferior parietal lobule (IPL, Brodmann areas 39 and 40). It is also known as Geschwind’s territory because the neurologist Geschwind predicted in the 1960s that the parietal lobe played a role in language, and was proven right when the IPL was found to include a second connection between Broca’s area and Wernicke’s area, which are of central importance in language. The IPL is very interesting as a part of the brain involved in synaesthesia because according to a 2004 article in New Scientist magazine the IPL matures at a late age, between the ages of five and seven years, which just happens to be time in life when children typically learn the ability to read and write, and it is also the age range in which some children develop grapheme-colour synaesthesia. I find this very interesting because in my family we have at least three closely related grapheme-colour synaesthetes who are unusually high achievers in reading and writing in testing and academic achievement. Two of these synaesthetes were early readers and also talented at language learning. What’s the betting that some gene that alters the development of the IPL is behind this? The author of the most interesting little science magazine article that brought me this news, Alison Motluk, is herself a synaesthete. Is it just a coincidence that a journalist with a well-connected brain has pointed out a number of interestingly related facts that are connected around the conceptual hub of the inferior parietal lobule?

Specht, Karsten Synaesthesia: cross activations, high interconnectivity, and a parietal hub. Translational Neuroscience. Volume 3 Number 1 (2012), 15-21, DOI: 10.2478/s13380-012-0007-z
http://www.springerlink.com/content/512306132j162437/

Croisile, Bernard Benson’s syndrome or Posterior Cortical Atrophy. Orphanet. September 2004. http://www.orpha.net/data/patho/GB/uk-Benson.pdf

Ward, Jamie, Sagiv, Noam and Butterworth, Brian The impact of visuo-spatial number forms on simple arithmetic. Cortex. Volume 45 Issue 10Pages 1261-1265 (November 2009). http://www.cortexjournal.net/article/S0010-9452(09)00213-5/abstract

Rouw, Romke, Scholte, H. Steven, Colizoli, Olympia Brain areas involved in synaesthesia: A review. Journal of Neuropsychology. Special Issue: Synaesthesia. September 2011 Volume 5 Issue 2 p.214-242. Article first published online: 16 SEP 2011 DOI: 10.1111/j.1748-6653.2011.02006.x  http://onlinelibrary.wiley.com/doi/10.1111/j.1748-6653.2011.02006.x/full

Motluk, Alison Two links good for kids’ language comphrehension. New Scientist. Issue 2478. December 18th 2004. p.12. http://www.newscientist.com/article/mg18424784.300-second-link-discovered-in-human-language-circuit.html