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Translating cell biology into therapeutic advances in Alzheimer's disease
Abstract
Studies of the molecular basis of Alzheimer's disease exemplify the increasingly blurred distinction between basic and applied biomedical research. The four genes so far implicated in familial Alzheimer's disease have each been shown to elevate brain levels of the self-aggregating amyloid-beta protein, leading gradually to profound neuronal and glial alteration, synaptic loss and dementia. Progress in understanding this cascade has helped to identify specific therapeutic targets and provides a model for elucidating other neurodegenerative disorders.
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Aβ is a 39-43-amino acid peptide derived from the proteolytic cleavage of the amyloid precursor protein (APP).
“A is a 39 -43-amino acid peptide derived from the proteolytic cleavage of the amyloid precursor protein (APP) (2).”
From Internalization of β-Amyloid Peptide by Primary Neurons in the Absence of Apolipoprotein E (2007) · cites this paper as [2]
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Metadata
- Authors
- Selkoe, D. J.
- Venue
- Nature
- Published
- 1999-06
- Volume
- 399
- Issue
- 6738
- Pages
- A23-A31
- ISSN
- 0028-0836
- 1476-4687
- Cited by
- 1,166
- References
- 24
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
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