an ALS Hypothesis - extended to all 'abnormal' neural atrophy

dag.stenberg at helsinki.nospam.fi dag.stenberg at helsinki.nospam.fi
Tue Feb 1 03:48:23 EST 2000


kenneth Collins <kpaulc at earthlink.net> wrote:
> i've reformatted my prior post to make online reading easier.

Ah, now it is all right.

Most points in your previous message are now clearly explained.
I think that (descrambled) hypothesis is quite worth to read. It may be
way off road, but at least the details and reasoning deserve thinking
about.

> the main thing that stimmed this 'dietary' stuff was with respect to the
> problem represented by the 'late onset' of the disease conditions, which
> needs explication. if, in accord with the traditional view, it actually
> is the case that a single DNA mutation results it the entirety of the
> disease condition(s), then why is it that the stuff of that mutation is
> activated in such a delayed way?

For comparison: in prion diseases, it takes times for anomalous PrP to
develop and for deposits to accumulate.

> >> i relied on the discussion of ALS in Kandel, et. al. for my 
> >> start. the factors that i found significant are as follows.

> >> the Hypothesis:

I had not earlier been able to find this among the over-long lines.

> >> the demyelination results from a specific brain stem lesion, 
> >> of a type analogous to the chemically-induced vestibular 
> >> lesion, or a stroke-induced lesion.
> >> ...

I do not see any explanation for the fact that brain stem symptoms are
usually later in appearance than limb involvement. It also seems to
neglect observable peripheral pathology.

> >> there are other attractive rationales for this sort of 
> >> hypothesis. the problem of the 35+ years typical onset of 
> >> ALS has to be explained. if there's a genetic flaw, then how 
> >> is it that it shows itself only after 35+ years? what's the 
> >> 'switch' that changes fully-functional motor neurons to
> >> dysfunctional 'motor' neurons?

Interesting question, no doubt.

> if this sort of thing occurs, then the disease is treatable through
> methods that eliminate the functionality of the newly-triggered stuff,
...
How would you diagnose the disease 35+ years before outbreak?

> at any rate, an explanation for the observed delayed onsets of
> Alzheimer's, ALS and Huntington's is necessary, and it will probably be
> the case that, when such delayed onset is explained, treatment
> strategies will become apparent within such explanation. so explication
> of the delayed onset is an important problem.

> >> the one criterion that =must= be met in order to explore 
> >> this hypothesis further is, since the ocular motor system is 
> >> not affected in ALS, to culture examples of ocular motor 
> >> neurons  along with examples of upper and lower motor 
> >> neurons, and look for differences that would allow the 
> >> ocular motor neurons to survive while the upper/lower motor 
> >> neurons would not survive.

This seems to me a profitable approach. Objections, anyone?

> i repeat, i'm taking this position in this hypothesis because all of the
> so-called 'indicators' that i've read of can result from excitotoxic
> activation, which means that it's possible that the 'indicators' are
> nothing of the kind, but 'only' by-products of a
> more-globally-correlated set of dynamics, such as those that i've been
> discussing in this hypothesis.

Logical. Not necessarily true, but logical.

> anyway, that's my contribution(?) to the efforts to extinguish these
> diseases. i could do more, but despite the fact that i've done this
> stuff at my own expense, i've only been 'ridiculed' for having tried

I think this (descrambled) hypothesis is quite worth to read. It may be
way off road, but at least the details and reasoning deserve thinking
about.

Dag Stenberg




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