Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease
By Jia Yao, R. Irwin, Liqin Zhao, J. Nilsen, Ryan T. Hamilton, R. Brinton. Proceedings of the National Academy of Sciences of the United States of America, 2009
915 citations recorded by the source corpus.
Subfields: Biological Psychiatry, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/10bc887ccf4099dcb195e0f09089a5c44643c8a9
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In Biological Psychiatry
- Bruce S. McEwen
- E. Nestler
- V. Krishnan
- Margaret A Sheridan
- J. Wingfield
- Nim Tottenham
- Sonia J. Lupien
- Andrew Steptoe
In Pharmacology
In Physiology
Citations in the corpus
- Neurobiological and Systemic Effects of Chronic Stress (2017, background): “Moreover, Abeta production is accelerated and Abeta oligomers enter into a vicious cycle leading to further damage,(11) and mitochondrial function declines under these conditions and contributes to the positive feedback cycle of toxicity.(64) With possible therapeutic potential, glucagon-like peptid”
- Mitochondrial dysfunction - the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicity (2011, methodology): “Mitochondrial dysfunction was evidenced by age-related decreased activity of regulatory enzymes of the oxidative phosphory lation system, and of PDH and COX in 3xTg-AD mice aged from 3 to 12 months [ 71 ].”
- Understanding the impact of sex and gender in Alzheimer's disease: A call to action (2018, neutral): “[98] Yao J, Irwin RW, Zhao L, Nilsen J, Hamilton RT, Brinton RD.”
- The mitophagy pathway and its implications in human diseases (2023, background): “Mitochondrial dysfunction, as reported, can precede the accumulation of Aβ deposits.(197,198) Normally functioning mitochondria can reduce aberrant amyloid precursor protein (APP) processing and the buildup of Aβ plaques.”
- Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “Cerebral glucose hypometabolism induced by dysfunction of oxidative phosphorylation is linked to AD pathophysiological alterations (Shoffner, 1997; Yao et al., 2009).”