ReviewOxidative medicine and cellular longevity2015
Mitochondrial Dysfunction Contributes to the Pathogenesis of Alzheimer's Disease.
Review in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
88 citing papers in PubMed, 142 citations in OpenAlex.
- Article
- Article
- Unraveling sex differences in age-related hippocampal decline: differential mitochondrial dysfunction, Lonp1-dependent mitochondrial proteostasis and mtROS production in aged C57BL/6 mice.Cell death & disease · 2025Article
- Insights into the Biomarker Potential of Humanin and Mots-c Expression and Telomere Length in Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Article
- Hippocampal mitophagy alterations in MAPT-associated frontotemporal dementia with parkinsonism.Acta neuropathologica communications · 2025Article
- Examining the role of antioxidant supplementation in mitigating oxidative stress markers in Alzheimer's disease: a comprehensive review.Inflammopharmacology · 2025Review
- A Mouse Model of Sporadic Alzheimer's Disease with Elements of Major Depression.Molecular neurobiology · 2025Article
- Plant food-derived antioxidant nutrients in neuroprotection against chemotherapy-induced neurotoxicity: from molecular mechanisms to clinical applications.Frontiers in nutrition · 2025Review
- Neuroprotection against beta-amyloid toxicity by the novel estrogen receptor modulator STX requires convergent signaling pathways.Frontiers in molecular neuroscience · 2025Article
- Mitochondrial plasticity and synaptic plasticity crosstalk; in health and Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Chronic Sustained Hypoxia Leads to Brainstem Tauopathy and Declines the Power of Rhythms in the Ventrolateral Medulla: Shedding Light on a Possible Mechanism.Molecular neurobiology · 2024Article
- Exosomal Dynamics and Brain Redox Imbalance: Implications in Alzheimer's Disease Pathology and Diagnosis.Antioxidants (Basel, Switzerland) · 2024Review
- Caspase-3 cleaved tau impairs mitochondrial function through the opening of the mitochondrial permeability transition pore.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- GlyNAC (Glycine and N-Acetylcysteine) Supplementation in Old Mice Improves Brain Glutathione Deficiency, Oxidative Stress, Glucose Uptake, Mitochondrial Dysfunction, Genomic Damage, Inflammation and Neurotrophic Factors to Reverse Age-Associated Cognitive Decline: Implications for Improving Brain Health in Aging.Antioxidants (Basel, Switzerland) · 2023Article
- Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Progranulin Deficiency Induces Mitochondrial Dysfunction in Frontotemporal Lobar Degeneration with TDP-43 Inclusions.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Article
- Unraveling the link: exploring the causal relationship between diabetes, multiple sclerosis, migraine, and Alzheimer's disease through Mendelian randomization.Frontiers in neuroscience · 2023Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease that affects millions of people worldwide. Currently, there is no effective treatment for AD, which indicates the necessity to understand the pathogenic mechanism of this disorder. Extracellular aggregates of amyloid precursor protein (APP), called Aβ peptide and neurofibrillary tangles (NFTs), formed by tau protein in the hyperphosphorylated form are considered the hallmarks of AD. Accumulative evidence suggests that tau pathology and Aβ affect neuronal cells compromising energy supply, antioxidant response, and synaptic activity. In this context, it has been showed that mitochondrial function could be affected by the presence of tau pathology and Aβ in AD. Mitochondria are essential for brain cells function and the improvement of mitochondrial activity contributes to preventing neurodegeneration. Several reports have suggested that mitochondria could be affected in terms of morphology, bioenergetics, and transport in AD. These defects affect mitochondrial health, which later will contribute to the pathogenesis of AD. In this review, we will discuss evidence that supports the importance of mitochondrial injury in the pathogenesis of AD and how studying these mechanisms could lead us to suggest new targets for diagnostic and therapeutic intervention against neurodegeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.