In article <1eh9kkINN8vo at pollux.usc.edu> jdevlin at pollux.usc.edu (Joseph T. Devlin) writes:
>Subject: Alzheimer's disease
>From: jdevlin at pollux.usc.edu (Joseph T. Devlin)
>Date: 19 Nov 92 23:57:08 GMT
>Keywords: Alzheimers, cognition, neuropathology
>Summary: Relating the neuropathology to cognitive deficits
>Hello all,
> I have been doing some research into the Alzheimer's
>literature and I characteristicly find a dichotomy between
>the cognitive deficits of AD and the known neuropathology
>of the disease. As yet I haven't seen even any suggestions
>as to how the two might relate.
Dear Joe:
At present there are speculations if Alzheimeres disease somehow relate
to oxidative destructions of brain tissue, and if antioxidants may prevent
such effects. Some recent litterature is listed:
1. Richardson, J. S., K. V. Subbarao, and L. C. Ang. 1992. On the
possible role of iron-induced free radical peroxidation in neural
degeneration in Alzheimer's disease. Ann.NY Acad.Sci. 648:326-327.
2. Backon, J. 1991. Dementia in cancer patients undergoing
chemotherapy: Implication of free radical injury and relevance to
Alzheimer disease. Med.Hypotheses 35:146-147.
3. Evans, P. H., J. Klinowski, and E. Yano. 1991. Cephaloconiosis: A
free radical perspective on the proposed particulate-induced
etiopathogenesis of Alzheimer's dementia and related disorders.
Med.Hypotheses 34:209-219.
Notes : By analogy to the etiology of the pneumoconioses, exogenous
dust-induced diseases of the lung, and endogenous crystal- induced
arthropathies such as gout, it is proposed that Alzheimer's dementia and
allied disorders are causally related to the accumulation of fibriform
inorganic deposits within the brain. Hence the neonosological term
'Cephaloconiosis'. It is proposed that: 1) either by the extrinsic migration
or intrinsic formation and deposition of insoluble and persistent inorganic
reactive nidi, the particle- induced generation of tissue-damaging
free-radical oxygen metabolites by stimulated brain glial macrophage-type
and allied phagocytic cells, provides a rationale for the etiopathogenesis
of neurodegenerative processes; 2) the modulation of the injurious
oxidative metabolic reaction by micronutrient and pharmacological
antioxidant agents is a rational and potentially feasible strategy for
future therapeutic clinical investigations. AUTHOR
4. Perrin, R., S. Brianon, C. Jeandel, Y. Artur, A. Minn, F. Penin, and G.
Siest. 1990. Blood activity of Cu/Zn superoxide dismutase, glutathione
peroxidase and catalase in Alzheimer's disease: A case-control study.
Gerontology 36:306-313.
5. Subbarao, K. V., J. S. Richardson, and L. C. Ang. 1990. Autopsy
samples of Alzheimer's cortex show increased peroxidation in vitro.
J.Neurochem. 55:342-345.
6. Volicer, L. and P. B. Crino. 1990. Involvement of free radicals in
dementia of the Alzheimer type: A hypothesis. Neurobiol.Aging
11:567-571.
Erik Lovaas
