Alzheimer's APP mangles mitochondria
Article Abstract:
A study was conducted to determine the way in which intracellular amyloid might cause cellular dysfunction, using post-mortem brain samples from human Alzheimer disease and control subjects. It was found that non-glycosylated full-length and C-terminally-truncated amyloid precursor protein was associated with mitochondria in samples from brains of individuals with Alzheimer disease, but not with mitochondria in samples from subjects without the disease.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2006
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Less stress, longer life
Article Abstract:
The oxidative stress theory of aging holds that the slow, steady accumulation of oxidative damage to macromolecules causes age-associated reductions in physiologic functions and reduces life expectancy. A corollary of the theory is that the rate of aging should be retarded by attenuation of oxidative damage and it is showed that overexpression of the antioxidant enzyme catalase in mitochondria extends lifespan in mice.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2005
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Merging mitochondria for neuronal survival
Article Abstract:
A pathological phenomenon types associated with mitochondrial fusion defects is explained based on a set of conditional knockout mice model with mitofusin 1 (Mfn1) or the Mfn2 genes. It suggests that loss of mitochondrial fusion induces a rapid degeneration of cerebellar Purkinje cells, which could lead to neurodegeneration.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2007
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