Reactive oxygen species-mediated loss of synaptic Akt1 signaling leads to deficient activity-dependent protein translation early in Alzheimer's disease

F Ahmad, K Singh, D Das, R Gowaikar… - Antioxidants & Redox …, 2017 - liebertpub.com
Aims: Synaptic deficits are known to underlie the cognitive dysfunction seen in Alzheimer's
disease (AD). Generation of reactive oxygen species (ROS) by β-amyloid has also been …

Reduced neuronal expression of synaptic transmission modulator HNK‐1/neural cell adhesion molecule as a potential consequence of amyloid β‐mediated oxidative …

SN Thomas, BA Soreghan, M Nistor… - Journal of …, 2005 - Wiley Online Library
Oxidative stress imparted by reactive oxygen species (ROS) is implicated in the
pathogenesis of Alzheimer's disease (AD). Given that amyloid β (Aβ) itself generates ROS …

Evaluation of mitochondrial oxidative stress in the brain of a transgenic mouse model of Alzheimer's disease by in vitro electron paramagnetic resonance spectroscopy

T Manabe, A Matsumura, K Yokokawa… - Journal of …, 2019 - content.iospress.com
Alzheimer's disease (AD) is one of the most common neurodegenerative diseases
responsible for progressive dementia. Deposition of amyloid-β (Aβ) in the brain is the most …

Oxidation of methionine 35 reduces toxicity of the amyloid beta-peptide (1–42) in neuroblastoma cells (IMR-32) via enzyme methionine sulfoxide reductase A …

F Misiti, ME Clementi, B Giardina - Neurochemistry international, 2010 - Elsevier
The beta amyloid peptide (Aβ), the major protein component of brain senile plaques in
Alzheimer's disease, is known to be directly responsible for the production of free radicals …

Endogenous reactive oxygen species cause astrocyte defects and neuronal dysfunctions in the hippocampus: a new model for aging brain

T Ishii, Y Takanashi, K Sugita, M Miyazawa… - Aging cell, 2017 - Wiley Online Library
The etiology of astrocyte dysfunction is not well understood even though neuronal defects
have been extensively studied in a variety of neuronal degenerative diseases. Astrocyte …

Alteration in glutathione content and associated enzyme activities in the synaptic terminals but not in the non-synaptic mitochondria from the frontal cortex of …

G Harish, A Mahadevan, MM Srinivas Bharath… - Neurochemical …, 2013 - Springer
Altered redox dynamics contribute to physiological aging and Parkinson's disease (PD). This
is reflected in the substantia nigra (SN) of PD patients as lowered antioxidant levels and …

Redox modifications in synaptic components as biomarkers of cognitive status, in brain aging and disease

P Muñoz, ÁO Ardiles, B Pérez-Espinosa… - Mechanisms of ageing …, 2020 - Elsevier
Aging is a natural process that includes several changes that gradually make organisms
degenerate and die. Harman's theory proposes that aging is a consequence of the …

Overexpression of glutathione peroxidase increases the resistance of neuronal cells to Aβ‐mediated neurotoxicity

M Barkats, S Millecamps, P Abrioux… - Journal of …, 2000 - Wiley Online Library
Senile plaques are neuropathological manifestations in Alzheimer's disease (AD) and are
composed mainly of extracellular deposits of amyloid β‐peptide (Aβ). Various data suggest …

Brain cytochrome oxidase activity and how it relates to the pathophysiology of memory and Alzheimer's disease

F Gonzalez-Lima, J Valla, A Čada - Free Radicals, Oxidative Stress, and …, 1998 - Springer
Recent studies indicate that mitochondrial electron transport dysfunction is involved in
various neurodegenerative diseases, including Alzheimer's disease. Although much …

Reduction in mitochondrial superoxide dismutase modulates Alzheimer's disease-like pathology and accelerates the onset of behavioral changes in human amyloid …

L Esposito, J Raber, L Kekonius, F Yan… - Journal of …, 2006 - Soc Neuroscience
Alzheimer's disease (AD) is associated with accumulations of amyloid-β (Aβ) peptides,
oxidative damage, mitochondrial dysfunction, neurodegeneration, and dementia. The …