it's not a Beta-amyloid thing

Kim kim at
Fri Jun 28 09:58:25 EST 2002

"Kenneth Collins" <k.p.collins at> wrote in
news:2NrS8.55528$LC3.4277696 at 

> it's not a Beta-amyloid thing. the Beta-amyloid thing happens be-cause
> 'normal' transcription is prematurely interrupted be-cause 'latching'
> neural dynamics are prematurely interrupted. for those who have AoK,
> it's a TD E/I-minimization "ratchet-pawling" [Ap5] deficit.
> the 'point' being that, researchers should look-elsewhere, a bit,
> starting by looking =carefully= for 'abnormally'-high-frequency
> 'EEG'-type traces. the sub-problem, here, is that the global EEG must
> be broken into 'component' sub-'parts' because the correlated
> 'abnormal' high-frequency trace[s] will be masked within the global
> trace, as the nervous system struggles to compensate with respect to
> the failing TD E/I-minimization dynamics.
> shouldn't be difficult to sort it out.
> it's definitely =not= a Beta-amyloid thing.

I would say that neurodegeneration in Alzheimers mouse models was a beta-
amyloid thing! Beta-amyloid is widely accepted as being toxic, to cell 
cultures, and to in vivo experiments. Neurodegeneration occurs when 
changes in APP processing lead to the accumulation of beta-amyloid which 
goes on to affect surrounding neurons and other tissues, through 
oxidative damage which affects many other signalling pathways leading 
ultimately to apoptosis. The important question is what is the switch in 
healthy people which leads to the production of beta-amyloid and 
consequent neurodegeneration.

AD therapies need to deal with either preventing this switch and hence 
the production of beta-amyloid (which already successfully exist, through 
secretase inhibitors and knockout mice models), or by preventing the 
actions of beta-amyloid once produced (for example antioxidants show 
clinical benefits in AD). So yes it is curable but by addressing the 
beta-amyloid problems.

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