Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage.

By M. Mańczak, M. Calkins, P. Reddy. Human Molecular Genetics, 2011

783 citations recorded by the source corpus.

Subfields: Molecular Biology, Nutrition and Dietetics, Physiology

View Paper: https://www.semanticscholar.org/paper/0e73bdab6af3c8e7fc8a892e9c8518da4ef48793

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. P. Reddy
2. E. Trushina
3. E. Tönnies
4. M. Mańczak
5. Yan Pang
6. Xianqun Fan
7. Xieyang Xu
8. M. Calkins

In Nutrition and Dietetics

1. Yan Pang
2. Xianqun Fan
3. Xieyang Xu

In Physiology

1. P. Reddy
2. Yan Pang
3. Xianqun Fan
4. Xieyang Xu
5. M. Calkins
6. M. Beal
7. E. Trushina
8. E. Tönnies

Citations in the corpus

• Mitochondrial Dysfunction in Neurodegenerative Diseases (2012, background): “Mutant htt binds to DRP1 and increases its GTPase activity, and similar effects have been reported in AD (Manczak et al., 2011).”
• Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease. (2011, background): “Protein changes in mitochondrial proteins (Drp1, Fis1, Mfn1, Mfn2 and Opa1) were also probed with western blot analysis (Fig.”
• 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].”
• Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “Moreover, DLP1 interacts with Aβ monomers and oligomers in AD brain, and these abnormal interactions are increased with disease progression [92], although it is not clear how such interaction affects DLP1 function and the balance of mitochondrial fission/fusion.”
• Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances (2025, positive): “354 In their subsequent study, they further demonstrated that Drp1 also interacted with p-tau in the brain of AD patients.”