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Zoology and wildlife conservation

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Abstracts » Zoology and wildlife conservation

Degeneration in vitro of post-mitotic neurons overexpressing the Alzheimer amyloid protein precursor

Article Abstract:

The role of beta/A4 amyloid protein precursor (APP) in the pathology of Alzheimer's disease was made clearer when APP was found to cause neuronal degeneration in mice. APP is a large membrane-bound glycoprotein that consists partly of amyloid fibrils. Deposits of these fibrils in the brain characterizes the pathophysiology of Alzheimer's. The finding that genetically overexpressed APP can affect post-mitotic neurons should stimulate further research linking APP with Alzheimer's disease and similar neuropathological disorders.

Author: Yoshikawa, Kazuaki, Aizawa, Takako, Hayashi, Yokichi
Publisher: Macmillan Publishing Ltd.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1992
Abnormalities, Physiological aspects, Amyloidosis, Neurons

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Neurotoxicity of beta-amyloid

Article Abstract:

The role of beta-amyloid plaques in the pathogenesis of Alzheimer's disease remains in dispute. Beta-amyloid precursor protein (APP) produces the abnormal deposits of beta-amyloid that are known to form in the brains of Alzheimer's patients. However, the conclusion that APP neurotoxicity starts the development of Alzheimer's disease could be strengthened by answering questions such as APP's effect on cultured neurons. However, another view is that amyloid deposits outside the neurons cause the neuronal degeneration.

Author: Martin, George M., Yoshikawa, Kazuaki, Fukuchi, Ken-ichiro, Sopher, Bryce
Publisher: Macmillan Publishing Ltd.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1993
Development and progression, Nervous system, Nerve degeneration

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New mice for old questions

Article Abstract:

Scientists Kuro-o's genetic research identifying the mutant klotho (kl) gene and its possible role in human pathology is interesting but not necessary likely. Kuro-o has managed to give a non-mutant phenotype to mice with a genetically-mutated kl genotype and suggests that kl is potent in the aging human genotype. However, a number of questions regarding beta-glucosidase gene domains must be answered before such a conclusion can be drawn.

Author: Martin, George M., Mian, I. Saira Mian
Publisher: Macmillan Publishing Ltd.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1997
Genetic aspects, Mutation (Biology), Mutation, Pathology

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Subjects list: Research, Alzheimer's disease
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