PLT Test Blog

This blog aims to synthesize the relevant parts of the research and make connections that point towards some potential therapeutic avenues.   Most researchers work in splendid isolation and concentrate on one extremely narrow area of interest. The GABA A reset, not functional in some autism On the one hand things are very simple, if the GABA A receptors function correctly and are inhibitory and the glutamate receptors (particularly NMDA and mGluRx) function correctly, there is harmony and a   perfect excitatory/inhibitory balance. Unfortunately numerous different things can go wrong and you could write a book about each one. As you dig deeper you see that the sub-unit make-up of GABA A receptors is not only critical but changes.   The plus side is that you can influence this. Today we see that the receptors themselves are physically movable and sometimes get stuck in the “wrong place”. When the receptors cluster close together they produce a strong inhibitory effect, but...

There was a rather complicated post in which I was linking some of the odd biological features of autism to something called RORα. This was one of those posts that appeals to the scientist readers like Tyler. The Purkinje-RORa-Estradiol-Neuroligin-KCC2 axis in Autism Happy with his elevated estradiol level Today’s post is more like the Psychiatrist's take on the same subject, so it is less complicated. I was thinking that a logical way to treat boys, post puberty, and girls with autism would be to target RORα. In males this would be the treating aromatase deficiency.   You would start by measuring by measuring the level of testosterone and estradiol in both boys and girls. My assumption is that there will be a substantial group of males who will have high testosterone and low estradiol.   In autism and its big brothers (and sisters) Schizophrenia and Bipolar, there are disturbed levels of these hormones.   One logical therapy would be estradiol, which is much less proble...

Researchers use animals in place of humans, for research purposes; in the case of autism it is usually the unfortunate mouse, but sometimes rats.   The Jackson Laboratory in the US is the source for more than 8,000 strains of genetically defined mice used for research purposes.      SFARIgene has a fascinating on-line database   that lists all the mouse/rat models of autism and the research linked to them. Most importantly it also lists all the “rescue lines”, the research showing therapies that improved the mouse’s autism.   For example, you can look up the model of human Fragile-X, which is called Fmr1, and then see the long list of drugs that helped that particular type of mouse.   There are already well over 200 different mouse/rat genetic models of autism and 1,000 rescue lines.    So while medicine has no approved drugs to treat human autism, autistic mice appear to be better placed. There remains the question of how close humans are t...

In my book I will be covering the science behind hopefully almost all autism, which then naturally leads to translating it into therapy.  In the ideal world you would just skip straight to the therapy and the final section of the book will be just that.  Clearly it would make sense to read the science first, so that you know what are the dysfunctions that you might need to treat. Hopefully there will also be some case studies from people who have applied a science-based approach to identify and implement effective therapies. Roger would clearly make a very good example of a reversible in-born metabolic-caused type of autism. I will be posting on my blog some drafts from the Part III - Translating Science to Treat Autism.  This is of course just one person's collection of other people's ideas and some of his one.  The reader and his/her medical medical team ultimately decide what to implement and must monitor its ongoing implementation.  * * *...