Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease.
By M. Calkins, M. Mańczak, P. Mao, U. Shirendeb, P. Reddy. Human Molecular Genetics, 2011
598 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/f5c73ec9be725f075df946ccb4c241b585054185
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Citations in the corpus
- Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “[97] also found fragmented mitochondria and an altered expression of mitochondrial fission/fusion proteins in primary neurons isolated Yan et al.”
- Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease (2017, background): “Further, increased levels of A could accelerate a production of ROS by directly binding to mitochondrial membranes, altering mitochondrial dynamics and function, ultimately leading to the abnormal energy metabolism and the loss of synaptic function [35, 37, 39, 46, 62, 125, 126].”