A new take on mental illness(Was Re: discovery of dopamine...)

David Bovee dbovee at phoebe.cair.du.edu
Sun Nov 19 00:20:50 EST 1995


>....
>Could it be that these diseases have causes oposite to the
>usual explaination.  Perhaps the resceptors for certain
>neurotransmitters are over expressed.  Maybe its this that
>causes a drop in neurotransmitter levels as the brain
>attempts to keep itself regulated.  Maybe low transmitter
>levels are not the cause of disfunction but a _result_
>of a more fundamental disfunction at the genetic
>transcription level.
>>j.e.cox at cranfield.ac.uk
>
>John E. Cox
>

	I doubt that you would find overexpression of neurotransmitters.  In 
fact, in Alzheimer's Disease, the neurophysical findings after death, aside 
from the diagnostic senile plaques and neurofibrillary tangles, include a 
decreased density of AChR, specifically of the nicotinic type.  This 
correlates with other work which indicates depressed levels of ACh in the 
CNS.
	Certainly, in this case, the problem is not overexpression 
effecting a regulatory mechanism.  Further, it is noteworthy that there is 
definately a genetic (hereditary) component to some cases of AD.  It has been 
shown that three different gene loci (on chromosomes 1, 14, and 21) are 
involved with AD, and in fact you may note that Down's syndrome also arises 
(most commonly) from a c21 abnormality.  I believe it has even been postulated 
that there is some potential relationship between Downs and AD.
	I think to address the issue, one needs to look at the pathologic 
mechanism.  The pathology somehow affects the homeastatic regulatory 
mechanisms, so the issue becomes one of pathologic control rather than the 
homeostatic control.

-- 
David Bovee
Dept. of Chemistry
University of Denver




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