Abstract
Calpains modulate processes that govern the function and metabolism of proteins key to the pathogenesis of Alzheimer's disease, including tau and amyloid precursor protein. Because activation of the calpain system might contribute to the impairment of synaptic transmission in Alzheimer's disease, we are currently testing the hypotheses that a treatment with calpain inhibitors might restore normal cognition and synaptic transmission in a transgenic model of Alzheimer's disease, the APP (K670N:M671L)/PS1(M146L) mouse. Findings derived from these studies will provide a novel approach to cognitive enhancement in Alzheimer's disease.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / enzymology
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Alzheimer Disease / genetics
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Amyloid beta-Protein Precursor / genetics
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Amyloid beta-Protein Precursor / metabolism
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Animals
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Calpain / antagonists & inhibitors*
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Calpain / metabolism
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Cysteine Proteinase Inhibitors / pharmacology*
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Cysteine Proteinase Inhibitors / therapeutic use
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Disease Models, Animal
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Hippocampus / drug effects*
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Hippocampus / enzymology
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Hippocampus / physiopathology
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Leucine / analogs & derivatives*
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Leucine / pharmacology*
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Leucine / therapeutic use
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / genetics
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Maze Learning / drug effects
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Maze Learning / physiology
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Membrane Proteins / genetics
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Membrane Proteins / metabolism
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Memory Disorders / drug therapy
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Memory Disorders / enzymology
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Memory Disorders / genetics
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Mice
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Mice, Transgenic
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Organ Culture Techniques
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Presenilin-1
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Treatment Outcome
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Up-Regulation / drug effects
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Up-Regulation / genetics
Substances
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Amyloid beta-Protein Precursor
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Cysteine Proteinase Inhibitors
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Membrane Proteins
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Presenilin-1
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Calpain
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Leucine
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E 64