PLT Test Blog

Today’s post is again about RORα, which was suggested to be a nexus where different biological dysfunctions that lead to autism may converge. I think you can consider RORα like a dimmer switch on your lights, you need to adjust the brightness to give the effect you want. Fine tuning ROR α to tune autism gene expression I recently came across some research where the scientist clearly has the same idea. He has been working on a synthetic RORα/γ agonist for some years and has investigated its use as both a cancer therapy and an autism therapy. I have become rather interested in cancer therapies because there are so many overlaps between what can lead to cancer and what exists in autism. The big research money is of course in cancer research. Tumor suppressor genes/proteins like PTEN and p53 have been shown to be disturbed in autism, as is Bcl-2. The Bcl-2 family of proteins regulate cell death ( apoptosis ) ; some members induce cell death and other inhibit it; the balance is important...

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...

Add testosterone/estradiol to those dysfunctional hormones This blog is about noticing connections and making things a little simpler to understand.   Today’s post is going to be a good example; all those odd sounding things like Purkinje cells and neuroligins all fitting nicely together. Today we see how a central hormonal dysfunction (testosterone/estradiol) can lead to an ion channel dysfunction (NKCC1/KCC2) at one end of the chain and at the other explains the absence of many Purkinje cells in the autistic cerebellum, which leads to some of the observed features of autism. I am calling it the Purkinje-RORa-Estradiol-Neuroligin-KCC2 axis, or Purkinje-KCC2 axis for short. We also get to see how melatonin fits in here and see why disturbed sleeping patterns should be expected in someone affected by the Purkinje- KCC2 axis. I should point out that not everyone with autism is likely affected by the Purkinje-NKCC1 axis, but I think it will apply to a majority of those with non-regre...