{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T09:04:37Z","timestamp":1790154277844,"version":"4.0.1"},"reference-count":51,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,11,15]],"date-time":"2012-11-15T00:00:00Z","timestamp":1352937600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008718","name":"Judith Jane Mason and Harold Stannett Williams Memorial Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008718","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp;amp; Dementia"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Synaptic dysfunction occurs early in Alzheimer's disease (AD) and is recognized to be a primary pathological target for treatment. Synapse degeneration or dysfunction contributes to clinical signs of dementia through altered neuronal communication; the degree of synaptic loss correlates strongly with cognitive impairment. The molecular mechanisms underlying synaptic degeneration are still unclear, and identifying abnormally expressed synaptic proteins in AD brain will help to elucidate such mechanisms and to identify therapeutic targets that might slow AD progression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Synaptosomal fractions from human autopsy brain tissue from subjects with AD (n = 6) and without AD (n = 6) were compared using two\u2010dimensional differential in\u2010gel electrophoresis. AD pathology is region specific; human subjects can be highly variable in age, medication, and other factors. To counter these factors, two vulnerable areas (the hippocampus and the temporal cortex) were compared with two relatively spared areas (the motor and occipital cortices) within each group. Proteins exhibiting significant changes in expression were identified (\u226520% change, Newman\u2010Keuls <jats:italic>P<\/jats:italic> value &lt; .05) using either matrix\u2010assisted laser desorption ionization time\u2010of\u2010flight or electrospray ionisation quadrupole\u2010time of flight mass spectrometry.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Twenty\u2010six different synaptic proteins exhibited more than twofold differences in expression between AD and normal subjects. These proteins are involved in regulating different cellular functions, including energy metabolism, signal transduction, vesicle transport, structure, and antioxidant activity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Comparative proteome analysis uncovered markers of pathogenic mechanisms involved in synaptic dysfunction.<\/jats:p><\/jats:sec>","DOI":"10.1016\/j.jalz.2012.04.009","type":"journal-article","created":{"date-parts":[[2012,11,13]],"date-time":"2012-11-13T05:32:08Z","timestamp":1352784728000},"page":"499-511","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["The synaptic proteome in Alzheimer's disease"],"prefix":"10.1002","volume":"9","author":[{"given":"Rachel Yoon Kyung","family":"Chang","sequence":"first","affiliation":[{"name":"School of Chemistry and Molecular Biosciences University of Queensland 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