Abstract
Synapse loss is one of the neuropathologies in Alzheimer's disease (AD) that may play a crucial role in the mechanism of its distinct cognitive impairment and dementia. In a previous study [18], a significant reduction of O-glycosylated clathrin assembly protein AP180 was observed in neocortex of AD. The reduction correlated with the density of neurofibrillary tangles. In this study we further determine that the O-GlcNAc/AP180 ratio is not changed, but the level of AP180 protein decreases in AD. Furthermore, whereas the level of neurofilament (NF-M) remains relatively unchanged, another clathrin assembly protein, AP-2, is also reduced in AD along with a small loss of synaptophysin. Our findings suggest that synaptic vesicle recycling dysfunction may be involved in the pathology of synapse loss in AD.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Acetylglucosamine / analysis
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Acetylglucosamine / metabolism
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Adaptor Proteins, Vesicular Transport
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Alzheimer Disease / metabolism*
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Alzheimer Disease / pathology
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Clathrin / metabolism*
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Enzyme Inhibitors / metabolism*
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Galactose / pharmacokinetics
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Glycosylation
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Humans
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Monomeric Clathrin Assembly Proteins*
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Nerve Tissue Proteins / isolation & purification
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Nerve Tissue Proteins / metabolism*
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Neurofibrillary Tangles / chemistry
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Neurofibrillary Tangles / metabolism
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Neurofilament Proteins / analysis
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Phosphoproteins / isolation & purification
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Phosphoproteins / metabolism*
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Precipitin Tests
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Synapses / chemistry
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Synapses / metabolism
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Synaptic Vesicles / chemistry
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Synaptic Vesicles / metabolism*
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Synaptophysin / analysis
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Tritium
Substances
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Adaptor Proteins, Vesicular Transport
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Clathrin
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Enzyme Inhibitors
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Monomeric Clathrin Assembly Proteins
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Nerve Tissue Proteins
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Neurofilament Proteins
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Phosphoproteins
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Synaptophysin
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clathrin assembly protein AP180
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Tritium
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neurofilament protein M
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Acetylglucosamine
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Galactose