{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T04:31:17Z","timestamp":1774326677812,"version":"3.50.1"},"reference-count":25,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2007,1,30]],"date-time":"2007-01-30T00:00:00Z","timestamp":1170115200000},"content-version":"vor","delay-in-days":2647,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Pineal Research"],"published-print":{"date-parts":[[1999,11]]},"abstract":"<jats:p><jats:bold>Abstract: <\/jats:bold> Most contemporary progress in Alzheimer's disease (AD) stems from the study of a 42\u201343 amino acid peptide, called the amyloid beta protein (A\u03b2), as the main neuropathologic marker of the disorder. It has been demonstrated that A\u03b2 has neurotoxic properties and that such effects are mediated by free\u2010radicals. Exposure of neuronal cells to A\u03b2 results in a spectrum of oxidative lesions that are profoundly harmful to neuronal homeostasis. We had previously shown that A\u03b225 35 induces oxidative damage to mitochondrial DNA (mtDNA) and that this modality of injury is prevented by melatonin. Because A\u03b225\u201035 does not occur in AD and because the mode of toxicity by A\u03b225\u201035 may be different from that of A\u03b21\u201042 (the physiologically relevant form of A\u03b2), we extended our initial observations to determine whether oxidative damage to mtDNA could also be induced by A\u03b21\u201042 and whether this type of injury is prevented by melatonin. Exposure of human neuroblastoma cells to A\u03b21\u201042 resulted in marked oxidative damage to mtDNA as determined by a quantitative polymerase chain reaction method. Addition of melatonin to cell cultures along with A\u03b2 completely prevented the damage. This study supports previous findings with A\u03b225\u201035, including a causative role for A\u03b2 in the mitochondrial oxidative lesions present in AD brains. Most important, the data confirms the neuroprotective role of melatonin in A\u03b2\u2010mediated oxidative injury. Because melatonin also inhibits amyloid aggregation, lacks toxicity, and efficiently crosses the blood\u2010brain barrier, this hormone appears superior to other available antioxidants as a candidate for pharmacologic intervention in AD.<\/jats:p>","DOI":"10.1111\/j.1600-079x.1999.tb00619.x","type":"journal-article","created":{"date-parts":[[2007,2,2]],"date-time":"2007-02-02T22:18:19Z","timestamp":1170454699000},"page":"226-229","source":"Crossref","is-referenced-by-count":72,"title":["Alzheimer \u03b2 protein mediated oxidative damage of mitochondrial DNA: Prevention by melatonin"],"prefix":"10.1111","volume":"27","author":[{"given":"M. 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