Burchell, VS and Gandhi, S and Deas, E and Wood, NW and Abramov, AY and Plun-Favreau, H (2010) Targeting mitochondrial dysfunction in neurodegenerative disease: Part II. EXPERT OPIN THER TAR , 14 (5) 497 - 511. 10.1517/14728221003730434.
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Areas covered in this review: This review examines the role of mitochondrial dysfunction in neurodegeneration, drawing examples from common diseases such as Alzheimer's disease and rarer familial disorders such as Charcot-Marie-Tooth. The review is provided in two parts. In part I we discussed the mitochondrial defects which have been most extensively researched (oxidative stress, bioenergetic dysfunction, calcium mishandling). We focus now on those defects which have more recently been implicated in neurodegeneration; in mitochondrial fusion/fission, protein import, protein quality control, kinase signalling and opening of the permeability transition pore.What the reader will gain: An examination of mitochondrial defects observed in neurodegeneration, and existing and possible future therapies to target these defects.Take home message: The mitochondrially-targeted therapeutics that have reached clinical trials so far have produced encouraging but largely inconclusive results. Increasing understanding of mitochondrial dysfunction has, however, led to preclinical work focusing on novel approaches, which has generated exciting preliminary data.
|Title:||Targeting mitochondrial dysfunction in neurodegenerative disease: Part II|
|Keywords:||Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, mitochondria, neurodegeneration, Parkinson's disease, therapeutics, PERMEABILITY TRANSITION PORE, NEUROBLASTOMA SH-SY5Y CELLS, SUPEROXIDE-DISMUTASE GENE, UBIQUITIN-LIGASE ACTIVITY, ACTIVATED PROTEIN-KINASE, CYTOCHROME-C RELEASE, PARKINSONS-DISEASE, ALZHEIMERS-DISEASE, OXIDATIVE STRESS, PINK1 FUNCTION|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Brain Sciences > Institute of Neurology > Molecular Neuroscience|
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