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James P. Bennett

Researcher at University of Virginia

Publications -  121
Citations -  9296

James P. Bennett is an academic researcher from University of Virginia. The author has contributed to research in topics: Mitochondrion & Mitochondrial DNA. The author has an hindex of 51, co-authored 121 publications receiving 8886 citations. Previous affiliations of James P. Bennett include Johns Hopkins University & University of Virginia Health System.

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Parkinson's Disease Brain Mitochondrial Complex I Has Oxidatively Damaged Subunits and Is Functionally Impaired and Misassembled

Paula M. Keeney, +3 more
- 10 May 2006 - 
TL;DR: Reduced complex I function in PD brain mitochondria appears to arise from oxidation of its catalytic subunits from internal processes, not from external oxidative stress, and correlates with complex I misassembly.
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Origin and functional consequences of the complex I defect in Parkinson's disease

Russell H. Swerdlow, +8 more
- 01 Oct 1996 - 
TL;DR: The complex I defect in PD appears to be genetic, arising from mitochondrial DNA, and may play an important role in the neurodegeneration of PD by fostering reactive oxygen species production and conferring increased neuronal susceptibility to mitochondrial toxins.
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An evaluation of the role of mitochondria in neurodegenerative diseases : mitochondrial mutations and oxidative pathology, protective nuclear responses, and cell death in neurodegeneration

David S. Cassarino, +1 more
- 01 Jan 1999 - 
TL;DR: This hypothesis, a synthesis of the mitochondrial mutations and oxidative stress hypotheses of neurodegeneration, is readily tested experimentally, and clearly points out many potential therapeutic targets for preventing or ameliorating these diseases.
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The parkinsonian neurotoxin MPP+ opens the mitochondrial permeability transition pore and releases cytochrome c in isolated mitochondria via an oxidative mechanism

David S. Cassarino, +3 more
- 06 Jan 1999 - 
TL;DR: MPP+ neurotoxicity may derive from not only its inhibition of complex I and consequent ATP depletion, but also from its ability to open the MTP and to release mitochondrial factors including Ca2+ and cytochrome c known to be involved in apoptosis.
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Cybrids in Alzheimer's disease: A cellular model of the disease?

Russell H. Swerdlow, +7 more
- 01 Jul 1998 - 
TL;DR: expression of unique functional characteristics relevant to neurodegeneration demonstrates the utility of these cells in defining AD pathophysiology at a cellular level and may prove useful in drug screening.