PLT Test Blog

A s we know, things often do not move fast in the world of medical research, at least when it comes to autism. Back in 2014 I wrote some posts about a novel immuno-modulatory therapy, based on TSO, a harmless gut parasite, developed for autism by one parent. He then shared it with Eric Hollander at The Albert Einstein College of Medicine. Then a small biotech company called Coronado, tried to develop TSO to treat a variety of inflammatory conditions, including autism. A pilot trial in autism was funded by the Simons Foundation and Coronado. Coronado did not achieve the desired results in their ulcerative colitis TSO trials, so their share price took a dive and they later changed their name to Fortress Biotech. It looks like they have given up on TSO. The autism Dad, Stewart Johnson, who originally came up with the idea has not updated his TSO website since 2011. http://autismtso.com/about/the_story/ I do wonder if he continues to give TSO to his son. The good thing is that he fully doc...

There are several old posts in this blog about the potential to treat some autism using statins; this has nothing to do with their ability to lower cholesterol.  Statins are broadly anti-inflammatory but certain statins do some other particularly clever things. This led me to use Atorvastatin and Fragile-X researchers to use Lovastatin. Fragile X is suggested by an elongated face and big/protruding ears;  other features include MR/ID and autism. I was recently forwarded a Scottish study showing why Simvastatin does not work in Fragile X syndrome, but Lovastatin does. Fragile X mental retardation protein ( FMR1 ) acts to regulate translation of specific mRNAs through its binding of eIF4E (see chart below). In people with Fragile X, they lack the FMR1 protein. Boys are worse affected than girls, because females have a second X chromosome and so a "spare" copy of the gene.           Simvastatin does not reduce ERK1/2 or mTORC1 activation in the Fmr1-/y hi...

A French Pyramid, worth visiting Today’s post is not full of complex science. I am reminded from time to time that I am supposed to be writing a book about translating autism science into practical therapy. To even partially do justice to all the science, things have to get a little complicated, at which point it will inevitably lose many readers. What is much easier to achieve is to explain what autism is, and is not, and what, if anything, you might want to do about it. I think you can consider autism as a hierarchy of impairments that together define a particular person’s “autism”.   For example, epilepsy is not just a comorbidity of someone’s autism, it is an integral part of it, and very much so biologically. All of this is a simplification, but I think it does actually help represent what is currently diagnosed as autism. Most people diagnosed today with autism are at the lower end of the pyramid/hierarchy, they have impaired social and communication skills to some degree and...

Open the above file via Google Drive, so it is big enough to read. Click the link below. You can also take links from it to the relevant blog post. https://drive.google.com/file/d/1Jl_JMUrX7suXz0n_yJPCLPinrvdddBhI/view?usp=sharing In the mini series of posts on ketones and autism we have come across a long list of effects that will benefit certain groups of people. 1.      Change in gut Bacteria 2.      Ketones as a brain fuel      3.      Niacin Receptor HCA2/ GPR109A 4.      NAD sparing 5.      CtBP Activation by reducing NADH/NAD+ ratio 6.      NLRP3 Inflammasome inhibition 7.      Class 1 HDAC inhibition 8.      Increase BDNF 9.      Ramification of Microglia 10. PKA activation 11. PPAR gamma activation It was interesting that the beneficial effect of the Ketogenic Diet in epilepsy i...