"Kenneth Collins" <k.p.collins at worldnet.att.net> wrote in
news:2NrS8.55528$LC3.4277696 at bgtnsc04-news.ops.worldnet.att.net:
> 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.
