Alzheimer's Disease and diagnosis w/ tropicamide (fwd)
x011 at Lehigh.EDU
x011 at Lehigh.EDU
Thu May 4 08:15:59 EST 1995
In article <799465407snz at longley.demon.co.uk>, David Longley <David at longley.demo
>In article <Pine.SGI.3.90.950501205152.10631A-100000 at umbc8.umbc.edu>
> rwashi1 at gl.umbc.edu "washington ryan" writes:
>>>>>>>>>>>>>>>C U T >>>>>>>>>>>>>>>>>
>> We give Alzheimer's patients medicine in an effort to increase their
>> acetylcholine production. They continue to decline.
>> Perhaps, we should do the opposite.
>> Give medicines to block acetylcholine transmission in the brain. The
>> brain should try to counteract the medicine by growing new acetylcholine
>> connections and reduce the process of erasing acetylcholine processing
>> sites. When we take the medicine away a month later the patient should
>> be performing at significantly higher levels of cognitive functions.
>> Ron Blue x011 at lehigh.edu
>Wouldn't this be akin to giving diabetics insulin receptor blockers, and
>parkinson's patients Dopamine receptor blockers in the hope that they would
>get better? I see the reasoning re: receptor supersensitivity etc, but ....
Yes, supersensitivity and possibly increase in receptor sites for
acetylcholine. If you have the model (GRIN!) of a bucket full of
water with a metal rod stuck in it and you are vibrating the bucket
at a particular frequency the metal rod messes up the waves on
the water. If you could use another procedure you may be able to
get a wave pattern that would normalize AS IF there were no metal rod
in the bucket.
The metal rod is symbolic of the process that lead to the destruction
of the hypocampus.
Using acetylcholine blockers may force the brain to destroy the area
destroying the hypocampus and increase in number of acetylcholine
When the acetylcholine blocker is removed the brain is functioning
at a more normal level.
Ron Blue x011 at lehigh.edu
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