it's not a Beta-amyloid thing

Kim kim at
Mon Jul 1 13:16:31 EST 2002

"Kenneth Collins" <k.p.collins at> wrote in
news:AAbT8.66991$UT.4611034 at 

> anyway, the main thing i'm doing in this thread is just working to get
> the 'point' across that =nothing= in molecular dynamics is
> disconnected from the neural-activation dynamics that're driven
> 'experientially'. 
> to the degree that they do so, all experiments that treat molecular
> stuff as being some sort of self-containing-code produce False
> results. 
> this's =not= saying the data they produce isn't Valuable. it is.
> it's just that the data is 'disconnected' from reality in a way that
> 'steers' folks away from being able to understand nervous system
> function. 
> it's like Functional Neuroanatomy before NDT's explication of
> "decussation' - all 'disconnected', and subject to widely-varying
> false hypotheses.
> i understand that this stuff must seem 'offensive', but that's only
> be-cause it's unfamiliar [even though i've been discussing it, in one
> form or another, since the early 1990s.]
> consider it until you get a 'handle' on it, and you'll see that it's
> an extraordinarily-useful organizing principle because it rigorously
> couples everything physically-internal with everything
> physically-external. one thing permeates everything: the one-way flow
> of energy from order to disorder that is what's described by 2nd
> Thermo [WDB2T]. 
> what this stuff does is lift the molecular stuff up from consisting of
> a bunch of abstract-ruleset stuff to being physically-coupled with
> external physical reality.
> once you See-it, you'll be able to make predictions re. the molecular
> stuff, do the experiments, and voila!
> eliminates a lot of the 'hunting-and-pecking',
> 'throwing-stuff-up-in-the-air-to-see-how-they-land, stuff.
> still, i understand that this stuff is, initially, 'offensive'.
> i mean no 'offense'.
> just the opposite.
> ken [k. p. collins]

I don't fully understand what it is that you are saying but I get the idea 
that you think that plaques are a result of neural dynamics that've 
'broken-down' elsewhere perhaps as a result of old-age through too much 
neural stimulation in a lifetime? Therefore using your neuronal networks 
too much stresses the cell which alters DNA/RNA which goes onto switch to 
beta-amyloid production and hence alzheimer's? which would explain partly 
why it is seen only in old age (Except with genetic mutations.).

With regard to the transgenic mouse models your theory would not apply as 
these mice have inherent genetic mutations (which are not present in aged 
humans) which bypass the "amyloid switching mechanism" in aged humans and 
produce amyloid regardless. I assume that you wish to apply your theory to 
the switching mechanism to the production of beta-amyloid, through which 
alzheimers disease manifests itself, in aged humans?

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