Tag Archives: Immune Hypothesis of Synesthesia

Surprising explanation for why face recognition matures unusually late in human development!

I didn’t expect to be reading this but I can recognize that this discovery seems to explain why face recognition is human cognitive ability that hits its peak surprisingly late in human development, and I’m now wondering how this fits into my theories about the relationship between my super-recognition and my synaesthesia, and that includes wondering how this discovery fits with my immune hypothesis of synaesthesia (which is all about pruning rather than proliferation), and of course I’m wondering how this fits in with what is known about super-recognizers. I guess I should just calm down and read the full text.

Coghlan, Andy Brain’s face recognition area grows much bigger as we get older. New Scientist. January 5th 2017.
https://www.newscientist.com/article/2117259-brains-face-recognition-area-grows-much-bigger-as-we-get-older/

Jesse Gomez, Michael A. Barnett, Vaidehi Natu, Aviv Mezer, Nicola Palomero-Gallagher, Kevin S. Weiner, Katrin Amunts, Karl Zilles, Kalanit Grill-Spector Microstructural proliferation in human cortex is coupled with the development of face processing. Science. January 6th 2017.

http://science.sciencemag.org/content/355/6320/68

 

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/

 

Amazed, not in a good way

The 2013 journal paper that ripped-off my excellent and original idea linking synaesthesia with specific elements of the immune system (published in this blog in 2012) has been reprinted as a chapter in a book that was published just a few months ago. One of the book’s authors is also one of the two authors of that paper, and another one of the book’s authors was an editor of that paper. Have these people no shame?

https://books.google.com.au/books?id=Tmy5CgAAQBAJ&source=gbs_navlinks_s

The offending paper has also been cited in a 2015 paper by two of the book’s authors

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403345/

Also not nice to know that recent work of those researchers was scheduled to be presented by one of them at the Eleventh Annual National Conference of the American Synesthesia Association at the University of Miami, Florida, held last month. This year’s conference was organized by the same academic who was the reviewer of the offending 2013 journal paper.

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

http://www.as.miami.edu/media/college-of-arts-and-sciences/content-assets/philosophy/docs/October%202-4%202015_Synesthesia_Program-miamiflorida.pdf

And one of those researchers will be the supervisor of a PhD studentship beginning January 2016

http://www.sussex.ac.uk/study/money/scholarships/pgr2016/view/541

I’d like to invite those involved (so many of them) to individually or collectively go and dip their left eyes in hot cocky cack, to quote an Australian cinema classic

http://aso.gov.au/titles/features/adventures-barry-mckenzie/clip1/?nojs=Ver

 

 

Wow, this is interesting

Scientists Find Vessels That Connect Immune System And Brain. June 3, 2015 | by Stephen Luntz. IFL Science.

http://www.iflscience.com/brain/vessels-found-connect-immune-system-and-brain

Structural and functional features of central nervous system lymphatic vessels

Antoine Louveau, Igor Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, Kevin S. Lee, Tajie H. Harris & Jonathan Kipnis
Nature (2015) doi:10.1038/nature14432
Received 30 October 2014 Accepted 20 March 2015 Published online 01 June 2015

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14432.html

I find this most interesting for a number of reasons. Firstly, the discovery showing that the human brain has functional lymphatic vessels connecting the brain with the immune system adds to a growing collection of evidence that the immune system plays important roles within the brain, which is an apparent partial violation of the long-held concept of the “blood-brain barrier” (as was described in a dated and inadequate chapter by Dr Karl in his 2013 pop science book Game of Knowns). In 2012 I was apparently the first person in the world, at this blog, to publish the ideas that high or low levels of the “component” immune chemicals at various points in development could be the cause of conditions of the brain such as developmental synaesthesia and Benson’s syndrome or PCA. My ideas were inspired by the very exciting research in areas such as microglia, complement, synaptic pruning and MHC1 molecules.

Another reason why this new discovery linking the central nervous system with the lymphatic and immune systems by researchers from the University of Virginia is so exciting is the fact that it is an unexpected discovery, as one might have thought that human anatomy would have already been thoroughly researched and discovered through the history of medical science to date, but then again, surprising new discoveries in human anatomy have not been unknown in recent years, with discoveries of new features in the human eye, knee and clitoris, the rediscovery last year of a major white matter tract (the vertical occipital fasciculus) at the rear of the brain that could play a central role in skills such as reading, and a new shape of neuron discovered in mouse brains. These new discoveries are exciting and also rather unsettling; exciting because it appears that important new discoveries in human neuroscience and anatomy are still possible, and unsettling because genuinely surprising new discoveries in science seem to indicate that science is not a steady accumulation of knowledge and a path of upward progress, as many believe. This may or may not be surprising to you, depending on which theory in the philosophy of science you favour. I think the discoveries of the VOF and the collection of discoveries about the roles and anatomy of the immune system in the human brain could be interpreted as evidence showing how incorrect ideas in science can become widely-accepted and widely-taught and could also have delayed the progress of new discoveries in neuroscience. How much further might we have come by now in our understanding of the human brain and mind if not for the popularity of the idea that the human brain is quarantined from the immune system? Which other influential ideas about the human brain are holding us back from a clearer understanding of the brain’s workings and diseases?

All those years of neuroimaging research on the brains of synaesthetes has found nothing of substance?

Hupé J and Dojat M (2015) A critical review of the neuroimaging literature on synesthesia. Frontiers in Human Neuroscience. 9:103.
doi:10.3389/fnhum.2015.00103

http://journal.frontiersin.org/article/10.3389/fnhum.2015.00103/abstract

“Our critical review therefore casts some doubts on whether any neural correlate of the synesthetic experience has been established yet”

That is a bit of a shock to read. This isn’t the first time that I’ve gotten a big shock after reading a paper in the journal Frontiers in Human Neuroscience. There was that little matter of some of my most amazing neuroscientific ideas published at this blog being ripped-off and used as the guts of an “opinion article” in that journal in 2013. I haven’t forgotten that episode. Who would have thought so much excitement is there to be found inside a science journal? I should make it clear that the researchers who did that thing in 2013 are NOT the authors of the above paper, but at the same time, I’ve got to wonder where Hupé and Dojat got this idea from

“…synesthesia could be reconsidered as a special kind of childhood memory, …”

Sure, they could have thought of that under their own steam, but I still want to point out that the central, seminal idea of this blog, right from the very first post in 2010, has been the idea that synaesthesia is linked in some meaningful way with face memory, in my case with super-recognizer ability in face memory, and there are many articles in this blog that show and hint that the heart of synaesthesia is memories created in childhood and many different types of synaesthesia operate in ways that are so much like memory that the differences are only quantitative. There was even one article published in 2013 at this blog in which I stated that

“…the Proust phenomenon is considered to be a type of memory and many of my observations at this blog have demonstrated that synaesthesia can involve memory, is an element of the “method of loci” memory technique and I would argue operates like memory. Yes, Yes, Yes, the Proust Phenomenon is a close relative of synaesthesia.”

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

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.

 

Finding confirmation of my beliefs and ideas, as you do

A closely related family member of mine recently scored a perfect mark on an adult literacy test geared to normal adults (which was true to form) , and another closely related family member in mid-childhood recently explained that they perceive motor vehicles as having faces and they categorize cars, utes and 4WDs into genders, square old 4WDs being male. I can see how that makes sense, but all the same I’ve never been that much of a car personifier. Ever since I was a child I’ve personified numbers and alphabet letters in great detail, along with perceiving them as essentially associated with very specific colours, and the shapes and motions of cars often make me think of hunting animals in some deeply instinctive way, but unlike my young relative and the many Australians who decorate their own motor vehicles with oversized curly eyelashes or giant imitation testes, I don’t see motor vehicles as male or female.

On the surface most people seem pretty-much normal and average, but if you make the most superficial investigation by testing or speaking with people about their thoughts and perceptions, you might find that there is an interesting and sometimes significant range of differences in the way our minds work. Grapheme-colour synaesthesia, personifying synaesthesia and elite and precocious levels of ability in reading, spelling and general literacy are just some of the interesting things that run in my family and are also experienced by me, and I am also a super-recognizer. A super-recognizer is a person who has an elite level of ability in recognizing faces or face memory, and typically can achieve perfect or near-perfect scores on tests of face memory. I believe that this co-occurrence of synaesthesia and elite abilities in face memory and literacy are no coincidence. I believe all of these things are based on hyper-connectivity or hyper-development in the rear parts of the brain including the fusiform gyrus, and also in the right hemisphere of the brain. I believe the genetic basis of this development might be linked to genes that code for particular variations in the functioning of the immune system, possibly involving the complement chemicals, microglia and synaptic pruning. I’m fascinated by the possibility that research work that has been done in the last decade linking immunology and neuropsychology can inform us about the origins of synaesthesia and also specific gifts and deficits in memory and cognition, and maybe also inform us about some types of dementia. In 2012 at this blog I explicitly identified research on the immune system, complement, microglia and synaptic pruning done by Dr Beth Stevens as a possible explanation for the origins of developmental synaesthesia, an idea that was so good that some synaesthesia researchers made it the basis of a speculative paper that was published in a peer-reviewed journal last year (they forgot to acknowledge me as the first to publish this idea). Work done on MHC1 (part of the immune system) and the brain by Carla Shatz is another area of scientific research that I find tremendously exciting, and I believe that the general area of research on the relationships between brain structure and the immune system is of such originality and importance that it should attract one or more Nobel Prizes.

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.

Action-packed YouTube video clip

Immune cell in the brain swallows synapses to sculpt neurons during development.

Posted by NIHNINDS (National Institute of Neurological Disorders and Stroke) at YouTube on May 22, 2012.

http://youtu.be/wb8UAyf8Nhw

The green thing is a mouse’s microglial cell. The movie is “courtesy Dorothy Schafer, Ph.D. and Beth Stevens, Ph.D. at Boston Children’s Hospital.” At this blog I have speculated that the kind of process shown in this brief video clip possibly happens less often in the brains of some people because they have lower levels of some of the complement chemicals that are a part of the immune system, with the result being the development of, or the retaining of, childhood or developmental synaesthesia. Some of the complement chemicals mark out synapses for destruction, I believe.

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.