it's not a Beta-amyloid thing

Kenneth Collins k.p.collins at
Fri Jun 28 14:21:36 EST 2002

Kim wrote in message ...
>"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.

such does not contradict anything in what i've posted.

>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.

i agree, but see the 'plaques' as a 'normal' consequence of the neural
dynamics through which molecular stuff is tightly-coupled to experience
being prematurely-disrupted.

what i'm saying is that the 'plaques' are 'only' a by-product of neural
dynamics that've 'broken-down' elsewhere.

i'm saying look-elsewhere to find the cause of the 'abnormal'
premature-disruption of 'normal' molecular dynamics. correct that
'elsewhere' stuff, and further by-production of the plaques will 'go away'

i'm saying that the looking-elsewhere can be approached via =differential=
'scanning' techniques ['EEG, to most-technologically-advanced].

>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.

again, what i'm saying is that seeing the plaques as 'the problem' misses
the stuff that'll, eventually, 'move toward' the Cure.

the plaques are not the result of some molecular-switch malfunction, but are
by-produced as a result of a break-down in more-globally-active neural
dynamics, through which the molecular stuff is 'normally' rigorously-coupled
with experience.

the 'break-down' is not at the molecular 'level'. it's at a higher 'level'
within the system as a whole.

the plaques are 'just' one detectable factor of a 'break-down' within these
more-globally-relevant, experientially-coupling,  neural dynamics.

the gist of my discussion has been, do the differential-scan stuff. find the
determining stuff. treat the determining stuff. the further production of
plaques will 'go away' [and, =maybe= reestablishment of 'normal' molecular
'time'-courses will also dis-integrate existing plaque-stuff. this last
possibility remains in question, in the perspective in which i work,
because, since the plaques are 'abnormal' stuff, the dynamics necessary for
their dissolution might not've been 'engineered' by evolutionary dynamics.
[why develop a 'tool' for a 'job' that "doesn't exist"? there're Infinite
such problems. so, if the Cure whose route i've proposed does issolve the
plaques, it'll be because the Cure, once established, inherently
reestablishes molecular dynamics that already exist, and that the plaques're
subject to such because they're 'just' incompleted 'normal' stuff.]]

Cheers, k. p. collins [ken]

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