it's not a Beta-amyloid thing

Kenneth Collins k.p.collins at
Thu Jun 27 19:59:41 EST 2002

Kenneth Collins wrote in message
<7dsS8.62906$UT.4294345 at>...
>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
>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 encour[a]ge folks to get on with this stuff, and can Guarantee
>Results. i've already Proven it in my noggin'-lab.

'course my methods are not tthose in-vogue among my Colleagues.

the easiest way to 'find your bearings' is the very-straight-forward
realization that =anything= that's unaffected by experience is unable to
Learn [unable to adapt] and is, therefore 'dead-weight', and to the degree
such exists, it drops a system cown in the survival hierarchy.

it's necessary to begin at such a Fundamental 'level' because doing so
enables one to gain initial insight which opens the 'door' to being able to
the necessary 'exploration' which so 'flies-in-the-face' of 'the way things
are supposed to be'. without such, the exploration is 'impossible' be-cause
it's relatively-unfamiliar, and, therefore, the TD E/I-minimization
mechanisms 'blindly' and automatically induce one to 'move away from' even
getting-started with the necessary exploration :-)

starting =simple= allows the simple insight's crystal-clarity to 'offset'
the biological mass correlated to that which has been long-familiar. there's
a 'catch' though. sustaining the simple thing requires elevation of the
"volitional diminishing-returns decision" threshold [AoK, Ap7, via
development of a correlated "prefrontal constellation". there's a lot of
Work, inherent, which is why the behavioral inertia of the 'status quo'
tends to be so strong. most folks'll 'bail-out', "calling the grapes 'sour',
anyway". "To hell with simple clarity." :-)

over the years, i've discussed everything that's necessary to take it all
the way.

at it's highest-'level' it all reduces to the one-way flow of energy from
order to disorder that is what's described by 2nd Thermo [WDB2T], which
Determines what Chemistry [Physics], and, therefore, what molecular
dynamics, can occur within nervous systems.

evolutionary dynamics 'engineer' everything in rigorous accord with WDB2T.

which, however many 'times' i say it, i expect reamins 'foreign' to just
about everyone.

which, i further expect, will remain as it is while folks 'move away from'
in-person discussion.


k. p. collins

>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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