Alzheimer's protein jams mitochondria of affected cells; resulting 'energy crisis' kills neurons

KP-PC k.p.collins at worldnet.att.net%remove%
Wed Apr 16 22:48:22 EST 2003


Hi John.

"John H." <johnh at faraway.xxx> wrote in message
news:3e9df39c at dnews.tpgi.com.au...
|
| http://www.eurekalert.org/pub_releases/2003-04/uop-apj040803.php
|
| Public release date: 14-Apr-2003
| [ Print This Article | Close This Window ]
|
| Contact: Steve Bradt
| bradt at pobox.upenn.edu
| 215-573-6604
| University of Pennsylvania
|
| Alzheimer's protein jams mitochondria of affected cells; resulting
'energy
| crisis' kills neurons
| PHILADELPHIA -- Opening a new front in the battle against
Alzheimer's
| disease, scientists at the University of Pennsylvania have found
that a
| protein long associated with the disease inflicts grave damage in a
| previously unimagined way: It seals off mitochondria in affected
neurons,
| resulting in an "energy crisis" and buildup of toxins that causes
cells to
| die. This pathway, the first specific biochemical explanation for
| pathologies associated with Alzheimer's, is detailed in the April
14 issue
| of the Journal of Cell Biology.

This is interesting, but [reserving the right to revise my reaction
if I ever get to read the article] it's only part of the story. There
has to be an explanation for the existence of the 'blocking' protein
that's traceable to a 'ramped' onset.

A skrewed-up protein still points back to skrewed-up transcription,
and, all in all, it still looks like the most-likely root
energydynamic is with respect to 'randomness' that reaches right into
transcription by failing to allow it to run to completion.

This'd result from the TD E/I-minimization conditions that I've
outlined in the past - which, with particular respect to this
article, is exciting because it provides a way to test the larger
hypothesis that I've been discussing [with respect to 'normal'
functioning] - that the 3-D energydynamics that're converged upon via
TD E/I-minimization reach right into the DNA, determining the
'momentary' activation of the DNA that becomes manifest in the
protein [which literally embodies the 3-D energydynamic through which
it's produced] that's transcribed.

If TD E/I-minimization is so "ephemeral" that, during the course of
transcription, the 3-D energydynamics that're imposed upon the DNA,
those 3-D energynamics alter beyond the 'normal' range of DNA
activation, the transcription will switch off before running to
completion, which'll leave an only-partially-formed protein.

This last thing is testable, at least to a degree - the
incompletely-formed protein should show a percentage 'similarity' to
the completely-formed protein that's 'normally' produced [it's not so
simple because it can also include stuff that's not in the 'normal'
protein [because, when the 'normal' 3-D energydynamics are
switched-off, that can result in an 'abnormal' transcription 'step'
because there'll be an 'abnormal' 3-D energydynamic transition - kind
of like what happens, say, during a conversational 'double-take' -
you know, a sentence that seemed 'appropriate', trailing-off
incompleted when it's been realized that it lacks 'appropriateness',
creating the existence of an 'abnormal' conversational transition
[stuff not in 'normal' conversation] - same-old, same-old, except for
TD E/I-minimization scale], but what's here should still be testable
on a percentage of 'normal'- and 'abnormal'-protein similarity.]

The larger hypothesis with respect to this stuff it that what's going
on is that TD E/I-minimization local to the transcription determines
the 3-D ionic conductances that present the 3-D energydynamics to the
DNA which determine the course of transcription.

This's very exciting because it constitutes a way to test what NDT
holds to be the case with respect to how TD E/I-minimization
'addresses' the DNA - a way to look right into, and verify, the 3-D
energydynamics that drive the DNA rigorously-coupling its 3-D
energydynamics to WDB2T.

As I've discussed in the past, since the the larger hypothesis
[discussed in former msgs] points directly to an amelioration regime,
if the test proposed here sustains the hypothesis, then that'd
'put-teeth' in the proposed Alheimer's amelioration strategy.

Perhaps I should write to the experimenter[s].

Can you see what I've discussed here?

If not, [all] please let me know so I can go over it in more detail.

This's important re. Alzheimers, but it could be a huge mother-load
of Treasure with respect to global nervous system function, in
particular, with respect to rigorously tying together global and
molecular energydynamics.

The first [easy?] step is to do the 'normal'-\'abnormal'-protein
percentage-of-similarity analyses.

Cheers, John, ken [K. P. Collins]





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