Alzheimer-like molecular pathology - due to repeated concussion?

[Guest guest]

There's an article in NYT on possible excess/early dementia among NFL

players.

It mentions this guy Andre Waters, who had a lot of neurologic

symptoms and committed suicide at age 44. His brain was examined by

one Omalu who reported finding the pathology of Alzheimer's.

Presumably he means a lot of it, as traces of this pathology are

found in most brains of (elderly, anyway) humans.

I found this abstract by Omalu, which refers to an NFL player other

than Waters:

" RESULTS: [...] There was mild neuronal dropout in the frontal,

parietal, and temporal neocortex. Chronic traumatic encephalopathy

was evident with many diffuse amyloid plaques as well as sparse

neurofibrillary tangles and [tau]-positive neuritic threads in

neocortical areas. There were no neurofibrillary tangles or neuropil

threads in the hippocampus or entorhinal cortex. Lewy bodies were

absent. The apolipoprotein E genotype was E3/E3. "

An interesting and broad review on amyloid in general (the beta

amyloid of Alz is not the only kind) is:

M.M. Picken, The changing concepts of amyloid, Arch Pathol Lab Med

125 (2001), pp. 38–43.

I got that Picken ref from Miklossy's paper on in vitro provocation

of beta amyloid by Bb. Citing Picken, Miklossy states:

" It has been known for almost a century that chronic bacterial

infection may lead to amyloid deposition in infected tissues and also

that amyloidosis can be induced by bacteria under experimental

conditions. "

Notice that we see beta amyloid in *response* to bacteria and perhaps

also trauma (which is immune activating), yet the bulk of work is

still focused on deranged amyloid production being " at the bottom of

it all. " These robust histological abnormalities can be a double

edged sword! While it sucks that we haven't even gotten off the dock

with CFS, with Alzheimer's we may have dropped anchor in shallow

water...