Inhibiting amyloid beta (1–42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex

Inhibiting amyloid beta (1–42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex

Increasing evidence suggests that mitochondrial dysfunction and aberrant release of mitochondrial reactive oxygen species (ROS) play crucial roles in early synaptic perturbations and neuropathology that drive memory deficits in Alzheimer’s disease (AD). We recently showed that solubilized human amyl...

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Bibliographic Details
Main Authors: Olayemi Joseph Olajide, Claudia La Rue, Andreas Bergdahl, Clifton Andrew Chapman
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-10-01
Series:Frontiers in Aging Neuroscience
Subjects:
Alzheimer’s disease
mitochondria
acetylcholine
entorhinal cortex
oxidative stress
reactive oxygen species
Online Access:https://www.frontiersin.org/articles/10.3389/fnagi.2022.960314/full

Internet

https://www.frontiersin.org/articles/10.3389/fnagi.2022.960314/full

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