kenneth Collins <kpaulc at earthlink.net> wrote:
> i've read enough to state, in a preliminary way, that the current focus
upon neural atrophy in the basal ganglia is 'ill-considered. as is
discussed in AoK, Ap5, the basal
> ganglia constitute a high-'level' supersystem configuration mechanism
that functions in accord with the TD E/I-minimization principle over
the relatively-long term.
Where do you find a "current focus upon... basal ganglia" in ALS
research??? Certainly not in the J.Neurosci article you cited.
> 1. this means that degeneration within the basal ganglia =must= be
correlated with wide-spread correlated observables, but in nothing
i've read, as yet, are such
> extra-striatal considerations addressed.
Don't understand. Focus in ALS is on lower motor neuron degenration in
the spinal cord, and on upper motor neuron degeneration but rather
elsewhere than in the basal ganglia, although there are indeed also reports
on basal ganglia involvement in a few cases.
> 2. the hypothesis that the striatal degeneration is a result of a
break-down in globally-ramifying TD E/I-minimization mechanisms has
You just wrote that the focus on basal ganglia is illconsidered. So why
worry about striatal degeneration.
> 4. i now extend the realm of this hypothesis to include =all=
'degenerative' diseases, including Huntington's, Parkinson's,
and the various Dystrophies.
Not surprised. But at the same time your theory becomes unusable for any
practical medical purposes.
> 5. all such diseases are variations on the single theme that was
discussed in the Alzheimer's hypothesis, with the variation being
correlated with differing
> 'points-of-failure' at levels below the diencephalon.
Well, in Alzheimer's the greatest problem is in the basal forebrain and
its neocortical projection, whereas in ALS the greatest problem is in
the spinal cord. Which "variation" are we now talking about here?
The rest was more or less a mess, so I leave it alone.
Please shorten your lines, they are about three times as long as my screen.