Increased mitochondrial fission and neuronal dysfunction in Huntington's disease: Implications for molecular inhibitors of excessive mitochondrial fission

Drug Discovery Today

Volumn 19, Issue 7, 2014, Pages 951-955

  Reddy, P Hemachandra ^a,b  

^a OREGON HEALTH AND SCIENCE UNIVERSITY   (United States)

^b OREGON HEALTH AND SCIENCE UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BRAIN DYSFUNCTION; DNA FRAGMENTATION; ENZYME ACTIVITY; FUSION GENE; HUNTINGTON CHOREA; MITOCHONDRIAL DNA REPLICATION; MITOCHONDRIAL DYNAMICS; MITOCHONDRIAL FISSION; MITOCHONDRIAL PERMEABILITY; MITOCHONDRION; NONHUMAN; OXIDATIVE PHOSPHORYLATION; PATHOGENESIS; REVIEW; ANIMAL; ANTAGONISTS AND INHIBITORS; DRUG EFFECTS; GENETICS; HUMAN; HUNTINGTON DISEASE; METABOLISM; MOLECULARLY TARGETED THERAPY; MUTATION; PHYSIOLOGY; PROCEDURES;

DNM1L PROTEIN, HUMAN; GUANOSINE TRIPHOSPHATASE; HTT PROTEIN, HUMAN; MICROTUBULE ASSOCIATED PROTEIN; MITOCHONDRIAL PROTEIN; NERVE PROTEIN;

ANIMALS; GTP PHOSPHOHYDROLASES; HUMANS; HUNTINGTON DISEASE; MICROTUBULE-ASSOCIATED PROTEINS; MITOCHONDRIAL DYNAMICS; MITOCHONDRIAL PROTEINS; MOLECULAR TARGETED THERAPY; MUTATION; NERVE TISSUE PROTEINS;

EID: 84903779388     PISSN: 13596446     EISSN: 18785832     Source Type: Journal    
DOI: 10.1016/j.drudis.2014.03.020     Document Type: Review

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