Abstract
Amyloid-beta (Abeta) peptides, found in Alzheimer's disease brain, accumulate rapidly after traumatic brain injury (TBI) in both humans and animals. Here we show that blocking either beta- or gamma-secretase, enzymes required for production of Abeta from amyloid precursor protein (APP), can ameliorate motor and cognitive deficits and reduce cell loss after experimental TBI in mice. Thus, APP secretases are promising targets for treatment of TBI.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid Precursor Protein Secretases / antagonists & inhibitors
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Amyloid Precursor Protein Secretases / deficiency
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Amyloid Precursor Protein Secretases / therapeutic use*
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Animals
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Aspartic Acid Endopeptidases / deficiency
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Brain Injuries / drug therapy*
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Brain Injuries / prevention & control
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Cognition / drug effects
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Disease Models, Animal
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Humans
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Mice
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Motor Activity / drug effects
Substances
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Amyloid Precursor Protein Secretases
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Aspartic Acid Endopeptidases
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Bace1 protein, mouse