{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T16:55:51Z","timestamp":1790268951976,"version":"4.1.0"},"reference-count":43,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2003,9,1]],"date-time":"2003-09-01T00:00:00Z","timestamp":1062374400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Geriatr Psychiatry Neurol"],"published-print":{"date-parts":[[2003,9]]},"abstract":"<jats:p>Neuropsychiatric manifestations are common in Alzheimer's disease (AD) and their phenotypic expression might be related to physiopathological and genetic causes. Multiple studies have implicated oxidative stress to the pathogenesis and possible etiology of AD. One of the mechanisms to protect cells from oxidative stress is the expression of heat-shock proteins (HSP). HSPA1B (alternatively known as HSP70-2) has been related to AD pathophysiology. In the present analysis, 77 AD patients were classified according to their cognitive status with the Neuropsychiatric Inventory and were genotyped for an insertion\/deletion (A1\/A2) polymorphism. The A2 allele conferred a significant increase of psychiatric morbidity in an allele-dose manner ( P &lt; .05). This pattern can be attributed to all AD stages and the severity of the behavioral disturbances was higher for those patients carrying one or two A2 alleles. These results indicate a possible association between the A2 allele and an overexpression of noncognitive symptoms in AD. 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