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

kenneth Collins kpaulc at earthlink.net
Thu Feb 3 13:45:16 EST 2000

BTW, except for the discussion of the specific 'lesion', everything in
the 'ALS' hypothesis that i've discussed has been in AoK, and the refs
cited in AoK, all along.

some of it, such as the schwan cell 'adjustments' of node of Ranvier
stuff, is 'implicit', though (in this case, in NDT's glial position,
which is in AoK).

AoK was written as an integrating 'overlay' with respect to the
traditional literature.

it's why it's been so 'heart'-breaking that AoK has been Censored. it's
integration of everything makes a =lot= of stuff relatively
straight-forward. (there's no way around coming to terms with the
details of the Neuroanatomy, however.)

i had to 'smile' as this 'ALS' hypothesis developed, because one of the
routine strategies that i used while developing NDT was to do
"thought-lesions" to the neural architecture, and 'watch' (literally)
the altered neural activation that happened as a result.

it's why the hypothesis came together so quickly (it was as it's been
presented when i posted the msg citing its "80%-verified" status, which
was early-on).

seems i had an "examples database" after all. developed it while
developing NDT, but never applied it to 'disease' conditions because i
"didn't think i could contribute" anything with respect to 'disease'

anyway, NDT (at the 'level' of AoK) allows the same thing to be done
with respect to lesions anywhere in the CNS.

it's why the theory is useful.

other matter: i'm not certain yet, but because i've still not found
employment, i might extend my ISP agreement so that i can have an online
presence with respect to finding employment.

ken (k. p. collins)

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