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Immunoexcitotoxicity — A unifying hypothesis
Serenoa
Posted: Monday, January 23, 2017 6:20 AM
Joined: 4/24/2012
Posts: 483


There is a curious similarity between Chronic Tramatic Encephelopathy (CTE) also known as "punch drunk" and Alzheimer's. I have been researching the known etiology of both and now believe they may be virtually the same disease. However the initial triggers leading to the shared pathology are different.  There are tantalizing clues, like the activation of APP on neurons after head trauma, the increase in levels of glutamate, restriction of blood flow in small blood vessels (ischemia), inflammatory response, high LDL and ApoE4 affects on arteries, the formation of hyperphosphorylated Tau. It is all coming together. The following article does a great job of revealing some of these very interesting connections.  

Immunoexcitotoxicity as a central
mechanism in chronic traumatic encephalopathy—A unifying hypothesis
Abstract
Some individuals suffering from mild traumatic brain injuries, especially repetitive mild concussions, are thought to develop a slowly progressive encephalopathy characterized by a  number of the neuropathological elements shared with various neurodegenerative diseases. A central pathological mechanism explaining the development of progressive neurodegeneration in
this subset of individuals has not been elucidated. Yet, a large number of studies indicate that a process called immunoexcitotoxicity may be playing a central role in many neurodegenerative diseases including chronic traumatic encephalopathy (CTE). The term immunoexcitotoxicity was
first coined by the lead author to explain the evolving patholo
gical and neurodevelopmental changes in autism and the Gulf War Syndrome, but it can be applied to a number of neurodegenerative disorders. The interaction between immune receptors within the central nervous system (CNS) and excitatory glutamate receptors trigger a series of events, such as
extensive reactive oxygen species/reactive nitrogen species generation, accumulation of lipid peroxidation products, and prostaglandin activation, which then leads to dendritic retraction,
synaptic injury, damage to microtubules, and mitochondrial suppression. In this paper, we discuss the mechanism of immunoexcitotoxicity and its link to each of the pathophysiological
and neurochemical events previously described with CTE, with special emphasis on the observed accumulation of hyperphosphorylated tau.

Lane Simonian
Posted: Monday, January 23, 2017 9:41 AM
Joined: 12/12/2011
Posts: 4779


Wonderfully done, Serenoa!  So many critical connections and observations in one place.