PLT Test Blog

Source: LDL receptor-related proteins 5 and 6 in Wnt/β-catenin signaling: Arrows point the way In earlier posts I have covered various signaling pathways such as Wnt, mTOR and the unusually sounding Hedgehog. You can go into huge detail if you want to understand these pathways, or just take a more superficial view. In most cases, things only start to go wrong if you are hypo/hyper (too little/too much) in these pathways. We saw with mTOR that most people with autism are likely to have too much activity and so might benefit from mTOR inhibition, but a minority will have the opposite status and stand to benefit from more mTOR activity. When it comes to Wnt signaling the research suggests the same situation. Wnt signaling is likely to be aberrant, but both extremes exist. Wnt signaling networks in autism spectrum disorder and intellectual disability Given the large volume of genetic data, analyzing each gene on its own is not a feasible approach and will take years to complete, let alone ...

I wrote several posts about why PAK1 inhibitors should be beneficial in some autism and indeed some schizophrenia. We also saw that PAK1-blocking drugs could be potentially useful for the treatment of neurofibromatosis type 2, in addition to RAS-induced cancers and neurofibromatosis type 1. One problem with drugs developed for cancer is that, even if they finally get approved, they tend to be ultra-expensive.  Production volumes are low because even if they “work” they do not prolong life for so long and cancer has numerous sub-types. Cheap drugs are ones used to treat common chronic conditions like high blood pressure, high cholesterol and indeed treatment of male lower urinary tract symptoms (LUTS), like benign prostatic hyperplasia (BPH). A small number of readers of this blog have confirmed the beneficial effect of PAK inhibitors in their specific sub-types of autism.  The problem is that there are no potent PAK1 inhibitors suitable for long term use that are readily avail...

  Very often the simplest solutions are the best and very often, when fault finding a problem, people overlook the obvious.   I seem to be forever having to mend things and I find this all the time. Back in 2013, when I knew much less about autism, I wrote about the experimental use of insulin like growth factor 1 ( IGF-1 ) in autism.   It’s a Small World – IGF-1 and NNZ-2566 in Autism It turned out that in autism the many different growth factors can be disturbed (too much, or too little) and this variation does indeed define some specific types of autism.  For example in Rett Syndrome there are very low levels of Nerve Growth Factor (NGF); low levels of NGF in some older people is the cause of their dementia.  In more common types of autism NGF is actually elevated. IGF-1 is very well studied.   IGF-1 is a primary mediator of the effects of   growth hormone   (GH).  Growth hormone is made in th e   anterior pituitary   ...

I have written several posts about Cinnamon and its metabolite Sodium Benzoate. I know that some readers are now using it for its cholesterol lowering and insulin sensitivity improving properties that were shown in the clinical trials I highlighted. Cinnamon and DJ-1 as a general Anti-Oxidant and perhaps Much More Is DJ-1 expression negatively associated with severity of Autism? If so, Sodium Benzoate (Cinnamon) may well be beneficial Sodium benzoate (Cinnamon) trialed for Schizophrenia (Adult-onset Autism) NMDAR hypo-function causing E/I imbalance in Autism and Schizophrenia – Baclofen, Sodium benzoate and Cinnamon (again) But has anyone tried it for autism? The first time I wrote about it I did acquire a big bag of the correct variety ( Cinnamomum verum or Ceylon Cinnamon) and also a bag of the very high flavanol ( epicatechin ) cocoa.  My cinnamon trial was limited to seeing what it looked/tasted like when added to the Polypill concoction Monty, aged 12 with ASD, drinks at brea...