PLT Test Blog

The Hungarian flag, for clever Laszlo Prokai     Lupron – partially right, but for the wrong reason?   In the US there undoubtedly are some quack therapies for autism, however on occasion we have seen that you can stumble upon an effective therapy for entirely the wrong reason. In the history of medicine there are drugs that were stumbled upon, or created by accident. In the case of the “Lupron protocol” which was promoted by a father and son (Geier and Geier), an extremely expensive therapy was apparently applied to hundreds of children, before being shut down by the medical regulators. Without going into all the details, Geier’s therapy combined chelation (antioxidants) and a drug called Lupron that causes a dramatic reduction in testosterone levels.   In the jargon, it causes h ypogonadism - diminished functional activity of the gonads ( the testes in males or the ovaries in females). Lupron is another of those drugs that costs ten times more in the US than in...

This post is best read if you have reviewed the earlier ones regarding the estradiol/testosterone disturbances in autism and how they govern the RORα “switch” that then triggers a torrent of other dysfunctions. So the hormonal disturbance, if present, is a key point at which to make a potent intervention.  The Purkinje-RORa-Estradiol-Neuroligin-KCC2 axis in Autism   Beauty is in the eye of the beholder In the mass media it is now popular to dismiss the fact that autism is far more prevalent on boys than girls. In the scientific literature, fortunately, they stick to the facts and much is written about the sex differences in autism. As we have seen in earlier posts, females have some natural defences against autism. They have two X chromosomes and of course they have those all-important neuroprotective female hormones (estrogen/estradiol, progesterone etc.). In effect, the more female you are, the more protection you have against idiopathic autism and any X-chromosome linked si...

Japan, home to today’s complicated research Today’s post hopes to give a more complete picture of the various processes involved in shifting the immature neurons often found in autism towards the mature neurons, found in most people.   This stalled process is complex and may only apply to around half of all autism. The post assumes prior knowledge from previous posts about the GABA switch and the KCC2 and NKCC1 chloride cotransporters. The best graphic I found is below and includes almost everything. The paper itself is very thorough and I recommend the scientists among you read the paper rather than my post. What we want to understand is why neurons did not switch from immature to mature, in the process I am calling the “GABA switch”.   We know a great deal about what happens before and after the switch and many processes that can be   involved, but the exact switch itself remains undefined. In a previous post I highlighted that neuroligin 2 (NL2)/RORa may be the GABA sw...