Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease.

By P. Reddy, M. Beal. Trends in Molecular Medicine, 2008

961 citations recorded by the source corpus.

Subfields: Biological Psychiatry, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/ec5ad22cf286e627ef53573322944a120c588b74

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. M. Calkins
2. M. Mańczak
3. P. Reddy
4. Junying Yuan
5. Wen Chen
6. Yongsheng Li
7. Ramnik J. Xavier
8. Huakan Zhao

In Physiology

1. M. Calkins
2. M. Mańczak
3. P. Reddy
4. P. Mao
5. Tao Lu
6. U. Shirendeb
7. B. Yankner
8. L. Reichardt

Citations in the corpus

• Genome-wide analysis reveals mechanisms modulating autophagy in normal brain aging and in Alzheimer's disease (2010, background): “Both excessive generation of ROS and accumulation of AVs are some of the earliest hallmarks of AD (4, 18, 19).”
• Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “181 Alterations in calcium homeostasis have also been observed among AD patients, which suggest that mitochondrial dysfunction may contribute to dysregulation of neuronal calcium levels in AD.”
• Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease. (2011, background): “Highly interrelated changes in mitochondria and synaptic function appear early in AD neurodegeneration (16,26).”
• 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. (2011, background): “A reduction in the clearance of Ab or the overproduction of Ab may lead to an accumulation of Ab in subcellular compartments of neuron, including mitochondria, endoplasmic reticulum, lysosomes and multiple vesicle bodies, and may impair functions of subcellular organelles and damage neurons (8,16).”
• Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease (2009, background): “Increased oxidative stress, coupled with dysregulation of calcium homeostasis and resulting apoptosis of vulnerable neuronal populations, are proposed to underlie the loss of synaptic activity and associated cognitive decline (9).”