In addition to Erik's list of references to AD, one might want to
check out:
Annals of Neurology (1992) V 32:Supplement
- this issue is devoted entirely to free radical involvement
in Parkinson's Disease
Mutation Research (1992) 275
- this issue is devoted entirely to metabolic failure due to
deletions in the mitochondrial genome
PD has clearer links between free radical damage and cell death
because the metabolism of dopamine results in the production of
H2O2. AD on the other hand appears to be a defect in protein
processing. One could speculate that a failure in protein
processing results in the accumulation of toxic products leading
to cell death. Of course high oxygen use causing free radical
damage to proteins and the lower levels of defenses found in AD
patients may help to accelerate the accumulation of proteins
which are not properly recycled.
All of this is compounded by the fact that we are slowly losing
our mitochondrial genome. Cells which consume large amounts
of oxygen and have poor defenses against free radicals (neurons)
are likely to suffer an increased rate of deletions to the
mitochondrial genome leading to energy insufficiency and
eventual cell death.
My feelings currently are that both AD and PD are probably a
genetic defect which interferes with the ability of particular
cells to deal with the damages caused by free radicals associated
with their individual biochemical environments.
--
Robert Bradbury uunet!sftwks!bradbury
Death is an imposition on the human race, and no longer acceptable
Alan Harrington, The Immortalist (1969)
