ReviewMolecular neurobiology2010
Mitochondrial dysfunction: common final pathway in brain aging and Alzheimer's disease--therapeutic aspects.
Review in Molecular neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
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Who cites it
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 243 citations in OpenAlex.
- Pooled it
- Toxicological effects of volatile organic compounds are mediated by aggravated oxidative stress and neuroinflammatory processes in piglets.Toxicology reports · 2026Article
- Mitochondrial dysfunction in peripheral mononuclear blood cells (PBMC) of individuals with mild cognitive impairment.GeroScience · 2026Observational
- Personalized functional topography-based multisite brain age prediction modeling reveals divergent neurodevelopment in major depression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Aerobic exercise improves astrocyte mitochondrial quality and transfer to neurons in a mouse model of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- 40 Hz light preserves synaptic plasticity and mitochondrial function in Alzheimer's disease model.Scientific reports · 2024Article
- DNA Damage and Parkinson's Disease.International journal of molecular sciences · 2024Review
- Article
- Mdivi-1 Rescues Memory Decline in Scopolamine-Induced Amnesic Male Mice by Ameliorating Mitochondrial Dynamics and Hippocampal Plasticity.Molecular neurobiology · 2023Article
- Combination of Secondary Plant Metabolites and Micronutrients Improves Mitochondrial Function in a Cell Model of Early Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Mitochondrial Bioenergetics, Redox Balance, and Calcium Homeostasis Dysfunction with Defective Ultrastructure and Quality Control in the Hippocampus of Aged Female C57BL/6J Mice.International journal of molecular sciences · 2023Article
- Antioxidant Intervention to Improve Cognition in the Aging Brain: The Example of Hydroxytyrosol and Resveratrol.International journal of molecular sciences · 2022Review
- Relationships ofNeurology. Genetics · 2022Article
- Secondary Mitochondrial Dysfunction as a Cause of Neurodegenerative Dysfunction in Lysosomal Storage Diseases and an Overview of Potential Therapies.International journal of molecular sciences · 2022Review
- Effects of Combining Biofactors on Bioenergetic Parameters, Aβ Levels and Survival in Alzheimer Model Organisms.International journal of molecular sciences · 2022Article
- Fatty Acids: A Safe Tool for Improving Neurodevelopmental Alterations in Down Syndrome?Nutrients · 2022Review
- Near-infrared light reduces β-amyloid-stimulated microglial toxicity and enhances survival of neurons: mechanisms of light therapy for Alzheimer's disease.Alzheimer's research & therapy · 2022Article
- Cross-species metabolomic analysis of tau- and DDT-related toxicity.PNAS nexus · 2022Article
- Walnut Oil Reduces Aβ Levels and Increases Neurite Length in a Cellular Model of Early Alzheimer Disease.Nutrients · 2022Article
- Role of Creatine Supplementation in Conditions Involving Mitochondrial Dysfunction: A Narrative Review.Nutrients · 2022Review
41 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
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a fully differentiated organ, our brain is very sensitive to cumulative oxidative damage of proteins, lipids, and DNA occurring during normal aging because of its high energy metabolism and the relative low activity of antioxidative defense mechanisms. As a major consequence, perturbations of energy metabolism including mitochondrial dysfunction, alterations of signaling mechanisms and of gene expression culminate in functional deficits. With the increasing average life span of humans, age-related cognitive disorders such as Alzheimer's disease (AD) are a major health concern in our society. Age-related mitochondrial dysfunction underlies most neurodegenerative diseases, where it is potentiated by disease-specific factors. AD is characterized by two major histopathological hallmarks, initially intracellular and with the progression of the disease extracellular accumulation of oligomeric and fibrillar beta-amyloid peptides and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. In this review, we focus on findings in AD animal and cell models indicating that these histopathological alterations induce functional deficits of the respiratory chain complexes and therefore consecutively result in mitochondrial dysfunction and oxidative stress. These parameters lead synergistically with the alterations of the brain aging process to typical signs of neurodegeneration in the later state of the disease, including synaptic dysfunction, loss of synapses and neurites, and finally neuronal loss. We suggest that mitochondrial protection and subsequent reduction of oxidative stress are important targets for prevention and long-term treatment of early stages of AD.
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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.