Patricia A. Trimmer

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.

TL;DR: Results provide potential mechanisms to support the feed‐forward hypothesis of Aβ neurotoxicity and increased intracellular Aβ levels can further exacerbate the genetically driven complex IV defect in sporadic Alzheimer's disease and may precipitate mitochondrial permeability transition opening.

TL;DR: Rec Recapitulation of defects previously observed in ALS subjects and ALS transgenic mice by expression of ALS mtDNA support a pathophysiologic role for mtDNA mutation in some persons with this disease.

TL;DR: The present study evaluates the time course of increased expression of the mRNA for glial fibrillary acidic protein (GFAP) within the dentate gyrus and hippocampus after unilateral lesions of the entorhinal cortex and shows that at 2 d postlesion, the levels of GFAP mRNA increased dramatically throughout the hippocampus bilaterally.

TL;DR: A precedent for inherited mtDNA mutation in some persons with PD is supported, present in cybrid lines containing mtDNA from maternal descendants with PD as well as in currently asymptomatic young maternal descendants.