Ability to delay neuropathological events associated with astrocytic MAO-B increase in a Parkinsonian mouse model: Implications for early intervention on disease progression

Neurobiology of Disease

Volumn 43, Issue 2, 2011, Pages 527-532

  Siddiqui, Almas ^a   Mallajosyula, Jyothi K ^b   Rane, Anand ^a   Andersen, Julie K ^a  

^a BUCK INSTITUTE FOR RESEARCH ON AGING   (United States)

^b ISIS PHARMACEUTICALS   (United States)

Author keywords

Mitochondrial complex I; Monoamine oxidase B; Parkinson's disease; Reactive oxygen species; Substantia nigra; Tyrosine hydroxylase

Indexed keywords

AMINE OXIDASE (FLAVIN CONTAINING) ISOENZYME B; ANTIOXIDANT; DOXYCYCLINE; EUK 189; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE DEHYDROGENASE (UBIQUINONE); UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIOXIDANT ACTIVITY; ASTROCYTE; CELL LEVEL; CELL LOSS; CONTROLLED STUDY; DISEASE COURSE; ENZYME ACTIVITY; ENZYME INDUCTION; ENZYME INHIBITION; ERRATUM; MOUSE; NERVE DEGENERATION; NEUROPATHOLOGY; NONHUMAN; OXIDATIVE STRESS; PARKINSONISM; PRIORITY JOURNAL; SUBSTANTIA NIGRA;

EID: 79958213681     PISSN: 09699961     EISSN: 1095953X     Source Type: Journal    
DOI: 10.1016/j.nbd.2010.12.014     Document Type: Erratum

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