{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T06:46:21Z","timestamp":1791269181403,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,6,28]],"date-time":"2004-06-28T00:00:00Z","timestamp":1088380800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2004,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The neurotoxin 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP) impairs mitochondrial respiration and damages dopaminergic neurons as seen in Parkinson's disease (PD). Here, we report that <jats:sc>L<\/jats:sc>\u20103\u2010hydroxyacyl\u2010CoA dehydrogenase type II\/amyloid binding alcohol dehydrogenase (HADH II\/ABAD), a mitochondrial oxidoreductase enzyme involved in neuronal survival, is downregulated in PD patients and in MPTP\u2010intoxicated mice. We also show that transgenic mice with increased expression of human HADH II\/ABAD are significantly more resistant to MPTP than their wild\u2010type littermates. This effect appears to be mediated by overexpression of HADH II\/ABAD mitigating MPTP\u2010induced impairment of oxidative phosphorylation and ATP production. This study demonstrates that HADH II\/ABAD modulates MPTP neurotoxicity and suggests that HADH II\/ABAD mimetics may provide protective benefit in the treatment of PD. Ann Neurol 2004;56:51\u201360<\/jats:p>","DOI":"10.1002\/ana.20133","type":"journal-article","created":{"date-parts":[[2004,6,28]],"date-time":"2004-06-28T17:06:17Z","timestamp":1088442377000},"page":"51-60","source":"Crossref","is-referenced-by-count":52,"title":["<scp>L<\/scp>\u20103\u2010hydroxyacyl\u2010CoA dehydrogenase II protects in a model of Parkinson's 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