The original place of publication (non-journal, non-academic, non-peer-reviewed) of the immune hypothesis of synesthesia or synaesthesia, by C. Wright, at this blog, in 2012, can be found at the link below.
The original place of publication (non-journal, non-academic, non-peer-reviewed) of the immune hypothesis of synesthesia or synaesthesia, by C. Wright, at this blog, in 2012, can be found at the link below.
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.
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.
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.
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.
I very much enjoyed watching Professor Peter Doherty AC FRS, Australian immunologist and Nobel laureate being interviewed on Lateline tonight about cuts to science funding and the CSIRO. Professor Doherty did some very important research involving the MHC proteins, which I believe have also been the focus of researchers interested in the development of the mammalian and human brain. I particularly liked Professor Doherty’s acknowledgement of the roles of citizen scientists in the science community, but I take issue a bit with his characterization of citizen scientists as generally people who have no training in science. There are plenty of people in the community who have academic achievements of various kinds in science or applied science who do not have paid jobs in science, for whatever reason. This doesn’t mean we aren’t educated or qualified or knowledgeable. Some voluntary roles in the community have more stringent training and screening processes than paid jobs, so the relationship between training and having a real job is also not absolute.
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?
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.