it's not a Beta-amyloid thing

Kenneth Collins k.p.collins at
Wed Jun 26 18:35:31 EST 2002

and, BTW, beyond the alleviation of Suffering and the maintainence of
quality-of-Life, and productivity, and elimination of 'warehouse'-type
'Medicine' costs, this's an =important= problem because, when it's Resolved,
experiential correlates will become Reified all the way down to the
most-molecular 'level' of nervous system function.

that is, TD E/I-minimization, which is already Verified in its
rigorous-correlations with experience, will seamlessly link-up with all
'molecular' Neuroscience's Stuff, rendering the molecular stuff also
rigorously-linked with experience.

that's a Worthy 'Goal'.

it's a good first-approach to getting-into-the nervous system, of-a-piece,
as it Exists, as a totally-integrated entity.

i'd volunteer to get it started, but i've no PhD, so i can't apply.

i've no hands-on experience 'in the lab'.

i do my 'lab' work in-my-head, while integrating the work of experimental

anyway, i encoursge folks to get on with this stuff, and can Guarantee the
Results. i've already Proven it in my noggin'-lab.

k. p. collins

Kenneth Collins wrote in message
<2NrS8.55528$LC3.4277696 at>...
>From: Kenneth Collins <k.p.collins at>
>Subject: Re: => 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'
>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
>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.
>Cheers, k. p. collins
> wrote in message ...
>>Postdoctoral Position as posted on the Postdoc Jobs website:
>>A Postdoctoral position is available to explore the regulation of Tau
>>and Beta-amyloid mediated neurodegeneration in transgenic mouse models
>>of Alzheimer's disease. The successful candidate must have
>>demonstrated knowledge in molecular neuroscience. Interested
>>candidates should send CV to: Dr. Giulio M. Pasinetti, Department of
>>Psychiatry, Mount Sinai School of Medicine, One Gustave L. Levy Place,
>>Box 1230, New York, NY 10029.
>>For more information, please visit Postdoc Jobs website:

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