it's not a Beta-amyloid thing

PF fell_spamtrap_in at ozemail.com.au
Thu Jun 27 11:37:41 EST 2002


"Kenneth Collins" <k.p.collins at worldnet.att.net> wrote in message
news:2NrS8.55528$LC3.4277696 at bgtnsc04-news.ops.worldnet.att.net...
> From: Kenneth Collins <k.p.collins at worldnet.att.net>
> Subject: Re: PostdocJobs.com => Neuroscience/Psychiatry
> Date: Wednesday, June 26, 2002 6:59 PM
>
> 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.
>
> the Beta-amyloid stuff occurs only as a by-product of the the failing TD
> E/I-minimization dynamics. the Beta-amyloid is what 'congeals-out-of'
> prematurely-interrupted transcription. [transcription that becomes
> 'supplanted' before it runs to completion.
>
> it's curable, but the necessary cure is with respect to the TD
> E/I-minimization deficit, not with respect to the Beta-amyloid stuff. fix
> the TD E/I-minimization deficit, and, to the degree of such, the
> Beta-amyloid abnormalities will go-away, and so will the symptomology.

I know what you are saying! I shall translate what you are saying into my
own, hopefully not too weird, words (if I can):

I believe Kenneth knows that the 'brainbodily bulk' of this (and many other)
problems consists of seriously accumulated neuromolecular consequences
(usually unconscious remembrances/residues) of some specific
life-situational stressor (or stressors) of _an adverse_ character (i.e.,
distressors rather than eustressors);

And, that when distress-mediating central neurons are revved (by an
individual's distress-motivating reality) too hard, too often, or too long,
these cells' DNA/RNA regulated manufacture of peptides and proteins tend to
brake down, something that can cause detrimental deposits -- remotely
similar to how an engine that is worked too hard build up deposits of soot.

This enormously important aspect of what is really going (of reality) is a
big part of what Arthur Janov has been trying to convey - in great, very
explicit, and in-your-face detail - to the community at large for about 35
years.

Peter





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