Science Features Neurodegeneration
Today's Science magazine, the house organ of AAAS, the American Association for the Advancement of Science, highlights the problem of neurodegeneration.
In the second paragraph in the lead article, it is stated, "Much fundamental research has led to a greater understanding of the pathophysiological processes involved in neurodegeneration and has revealed that accumulation of misfolded, toxic proteins is frequently a cause of neurodegeneration."
The "accumulation of misfolded, toxic proteins is frequently a cause of neurodegeneration." Will the Anavex sigma-1 receptor agonists treat or prevent protein misfolding? Strong evidence that they do, by optimizing the biochemical processes in endoplasmic reticula, the cellular location of protein folding.
An article made this claim: "Disrupted sleep often occurs before or in the early stages of neurogenerative disease. An important function of sleep is to allow waste products — including misfolded proteins associated with neurodegeneration — to be cleared from the brain via the glymphatic system."
It is noted that improved sleep has been a clinical outcome of those taking blarcamesine in early clinical trials.
The article elaborates on the crucial importance of functional autophagy, the ability of neurons to collect and reprocess waste proteins. Facilitated, optimized autophagy has been noted with blarcamesine.
Note the diseases referred to in this statement: "In addition to the deterioration of sleep architecture in aging, the neurodegenerative diseases — including AD, Parkinson’s disease, Huntington’s disease, the multisystem atrophies, and the FTDs — are all associated with sleep disturbances." Anavex is targeting AD (Alzheimer's disease), a form of Parkinson's disease, and FTD, frontotemporal dementia.
It will be an error to discount or dismiss the ability of blarcamesine to improve sleep.
The issue has many pages discussing the aggregation of the pathogenic proteins of Parkinson's disease, Alzheimer's disease, and other CNS diseases. Doubtless, the aggregation of these proteins cause their associated diseases. But I didn't find any discussion of how neurons might be treated so as to prevent waste protein aggregation. That's where blarcamesine will come into play, with it's ability of facilitate and promote normalized sigma-1 receptor protein functions; which include proper folding of proteins (enzymes) that clear waste proteins in earlier, more healthy stages of life.
An article deliberated on the genetics of Alzheimer's disease. But I note that except in some rather rare forms of Alzheimer's, the disease is late-onset. Until late middle age or later, even with "bad genes," the disease is not present. Can blarcamesine maintain a more youthful, functional status in nerves, preventing the geriatric onset of the disease? Let's see how the Alzheimer's clinical trial turns out.
In a few years, I expect another issue of Science to be devoted to neurodegeneration: "Sigma-1 Receptor Activation Terminates Neurodegeneration."
