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• W2989340731 abstract "Synaptic dysfunction is an early pathogenic event in Alzheimer disease (AD) that contributes to network disturbances and cognitive decline. Some synapses are more vulnerable than others, including the synapses of the perforant path, which provides the main excitatory input to the hippocampus. To elucidate the molecular mechanisms underlying the dysfunction of these synapses, we performed an explorative proteomic study of the dentate terminal zone of the perforant path. The outer two-thirds of the molecular layer of the dentate gyrus, where the perforant path synapses are located, was microdissected from five subjects with AD and five controls. The microdissected tissues were dissolved and digested by trypsin. Peptides from each sample were labeled with different isobaric tags, pooled together and pre-fractionated into 72 fractions by high-resolution isoelectric focusing. Each fraction was then analyzed by liquid chromatography-mass spectrometry. We quantified the relative expression levels of 7322 proteins, whereof 724 showed significantly altered levels in AD. Our comprehensive data analysis using enrichment and pathway analyses strongly indicated that presynaptic signaling, such as exocytosis and synaptic vesicle cycle processes, is severely disturbed in this area in AD, whereas postsynaptic proteins remained unchanged. Among the significantly altered proteins, we selected three of the most downregulated synaptic proteins; complexin-1, complexin-2 and synaptogyrin-1, for further validation, using a new cohort consisting of six AD and eight control cases. Semi-quantitative analysis of immunohistochemical staining confirmed decreased levels of complexin-1, complexin-2 and synaptogyrin-1 in the outer two-thirds of the molecular layer of the dentate gyrus in AD. Our in-depth proteomic analysis provides extensive knowledge on the potential molecular mechanism underlying synaptic dysfunction related to AD and supports that presynaptic alterations are more important than postsynaptic changes in early stages of the disease. The specific synaptic proteins identified could potentially be targeted to halt synaptic dysfunction in AD." @default.
• W2989340731 created "2019-11-22" @default.
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• W2989340731 date "2020-01-01" @default.
• W2989340731 modified "2023-09-30" @default.
• W2989340731 title "The Proteome of the Dentate Terminal Zone of the Perforant Path Indicates Presynaptic Impairment in Alzheimer Disease" @default.
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• W2989340731 cites W1983169045 @default.
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• W2989340731 cites W1990659183 @default.
• W2989340731 cites W1991886821 @default.
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• W2989340731 cites W2026060908 @default.
• W2989340731 cites W2028673251 @default.
• W2989340731 cites W2038963685 @default.
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• W2989340731 cites W2060384627 @default.
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• W2989340731 cites W2078653286 @default.
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• W2989340731 cites W2087243986 @default.
• W2989340731 cites W2087633823 @default.
• W2989340731 cites W2089936534 @default.
• W2989340731 cites W2097149810 @default.
• W2989340731 cites W2106931873 @default.
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• W2989340731 cites W2138885237 @default.
• W2989340731 cites W2154626303 @default.
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• W2989340731 cites W2271127896 @default.
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• W2989340731 doi "https://doi.org/10.1074/mcp.ra119.001737" @default.
• W2989340731 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6944231" @default.
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• W2989340731 hasPublicationYear "2020" @default.
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