{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T22:49:33Z","timestamp":1792968573947,"version":"4.5.0"},"reference-count":28,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2001,12,25]],"date-time":"2001-12-25T00:00:00Z","timestamp":1009238400000},"content-version":"vor","delay-in-days":542,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2000,7]]},"abstract":"<jats:p>\n                    <jats:bold>Abstract<\/jats:bold>\n                    : Inhibition of proteasome activity is sufficient to induce neuron degeneration and death ; however, altered proteasome activity in a neurodegenerative disorder has not been demonstrated. In the present study, we analyzed proteasome activity in short\u2010postmortem\u2010interval autopsied brains from 16 Alzheimer's disease (AD) and nine age\u2010 and sex\u2010matched controls. A significant decrease in proteasome activity was observed in the hippocampus and parahippocampal gyrus (48%), superior and middle temporal gyri (38%), and inferior parietal lobule (28%) of AD patients compared with controls. In contrast, no significant decrease in proteasome activity was observed in either the occipital lobe or the cerebellum. The loss of proteasome activity was not associated with a decrease in proteasome expression, suggesting that the proteasome may become inhibited in AD by a posttranslational modification. Together, these data indicate a possible role for proteasome inhibition in the neurodegeneration associated with AD.\n                  <\/jats:p>","DOI":"10.1046\/j.1471-4159.2000.0750436.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T01:46:09Z","timestamp":1047433569000},"page":"436-439","source":"Crossref","is-referenced-by-count":718,"title":["Impaired Proteasome Function in Alzheimer's Disease"],"prefix":"10.1111","volume":"75","author":[{"given":"Jeffrey N.","family":"Keller","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keith B.","family":"Hanni","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William R.","family":"Markesbery","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2001,12,25]]},"reference":[{"key":"e_1_2_5_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0891-5849(94)00244-E"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1460-9568.1999.00451.x"},{"key":"e_1_2_5_5_2","unstructured":"BraakH.&BraakE.(1994)Pathology of Alzheimer's disease inNeurodegenerative Diseases(Calne D. 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