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

> 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

Dag Stenberg

More information about the Neur-sci mailing list

Send comments to us at biosci-help [At] net.bio.net