Mitophagy and Alzheimer's Disease: Cellular and Molecular Mechanisms
Research output: Contribution to journal › Review › Research › peer-review
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Mitophagy and Alzheimer's Disease : Cellular and Molecular Mechanisms. / Kerr, Jesse S.; Adriaanse, Bryan A.; Greig, Nigel H.; Mattson, Mark P.; Cader, M. Zameel; Bohr, Vilhelm A.; Fang, Evandro F.
In: Trends in Neurosciences, Vol. 40, No. 3, 2017, p. 151-166.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - Mitophagy and Alzheimer's Disease
T2 - Cellular and Molecular Mechanisms
AU - Kerr, Jesse S.
AU - Adriaanse, Bryan A.
AU - Greig, Nigel H.
AU - Mattson, Mark P.
AU - Cader, M. Zameel
AU - Bohr, Vilhelm A.
AU - Fang, Evandro F.
PY - 2017
Y1 - 2017
N2 - Neurons affected in Alzheimer's disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid beta peptide (Aβ) and Tau pathologies. Emerging findings suggest that the autophagy/lysosome pathway that removes damaged mitochondria (mitophagy) is also compromised in AD, resulting in the accumulation of dysfunctional mitochondria. Results in animal and cellular models of AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contributes to synaptic dysfunction and cognitive deficits by triggering Aβ and Tau accumulation through increases in oxidative damage and cellular energy deficits; these, in turn, impair mitophagy. Interventions that bolster mitochondrial health and/or stimulate mitophagy may therefore forestall the neurodegenerative process in AD.
AB - Neurons affected in Alzheimer's disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid beta peptide (Aβ) and Tau pathologies. Emerging findings suggest that the autophagy/lysosome pathway that removes damaged mitochondria (mitophagy) is also compromised in AD, resulting in the accumulation of dysfunctional mitochondria. Results in animal and cellular models of AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contributes to synaptic dysfunction and cognitive deficits by triggering Aβ and Tau accumulation through increases in oxidative damage and cellular energy deficits; these, in turn, impair mitophagy. Interventions that bolster mitochondrial health and/or stimulate mitophagy may therefore forestall the neurodegenerative process in AD.
U2 - 10.1016/j.tins.2017.01.002
DO - 10.1016/j.tins.2017.01.002
M3 - Review
C2 - 28190529
AN - SCOPUS:85012907718
VL - 40
SP - 151
EP - 166
JO - Trends in Neurosciences
JF - Trends in Neurosciences
SN - 0378-5912
IS - 3
ER -
ID: 188451689