ReviewBiomolecules2024
Mitochondrial Dysfunction as the Major Basis of Brain Aging.
Review in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed.
- Targeting the FOXO4-p53 axis by retro-inverso peptide senolytic agents: a pharmacological strategy to mitigate brain aging and cognitive decline.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- FTO-mediated m6A demethylation regulates PGC-1α-dependent mitochondrial biogenesis to attenuate aluminum-induced neuronal senescence.Scientific reports · 2026Article
- Article
- The cellular choreography of brain aging: a neuroimmune network perspective.Frontiers in aging neuroscience · 2026Review
- Ageing, Neurodegeneration and the Endocannabinoid System.Current topics in behavioral neurosciences · 2026Review
- AUF1 Restrains Hepatocyte Senescence by Maintaining Mitochondrial Homeostasis in AML12 Hepatocyte Model.Cells · 2025Article
- Stress and neurodegeneration: mechanistic insights and therapeutic opportunities for preserving brain resilience.Acta neurologica Belgica · 2025Review
- Stimulatory Effects of (+)-Epicatechin on Short- and Long-Term Memory in Aged Rats: Underlying Mechanisms.Nutrients · 2025Article
- Early life stress, psychiatric conditions, and mitochondrial DNA copy number (mtDNAcn) in medically healthy young adults.Psychoneuroendocrinology · 2025Article
- Exercise orchestrates systemic metabolic and neuroimmune homeostasis via the brain-muscle-liver axis to slow down aging and neurodegeneration: a narrative review.European journal of medical research · 2025Review
- Curcumin nanoparticles alleviate brain mitochondrial dysfunction and cellular senescence in γ-irradiated rats.Scientific reports · 2025Article
- The Critical Role of Autophagy and Phagocytosis in the Aging Brain.International journal of molecular sciences · 2024Review
- Review
- Alzheimer's Disease, Obesity, and Type 2 Diabetes: Focus on Common Neuroglial Dysfunctions (Critical Review and New Data on Human Brain and Models).Brain sciences · 2024Review
- Harnessing BDNF Signaling to Promote Resilience in Aging.Aging and disease · 2024Review
- The Vital Role of Melatonin and Its Metabolites in the Neuroprotection and Retardation of Brain Aging.International journal of molecular sciences · 2024Review
- Mitophagy in Age-Dependent Neurodegeneration.Acta naturaeArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The changes in the properties of three biological events that occur with cerebral aging are discussed. These adverse changes already begin to develop early in mid-life and gradually become more pronounced with senescence. Essentially, they are reflections of the progressive decline in effectiveness of key processes, resulting in the deviation of essential biochemical trajectories to ineffective and ultimately harmful variants of these programs. The emphasis of this review is the major role played by the mitochondria in the transition of these three important processes toward more deleterious variants as brain aging proceeds. The immune system: the shift away from an efficient immune response to a more unfocused, continuing inflammatory condition. Such a state is both ineffective and harmful. Reactive oxygen species are important intracellular signaling systems. Additionally, microglial phagocytic activity utilizing short lived reactive oxygen species contribute to the removal of aberrant or dead cells and bacteria. These processes are transformed into an excessive, untargeted, and persistent generation of pro-oxidant free radicals (oxidative stress). The normal efficient neural transmission is modified to a state of undirected, chronic low-level excitatory activity. Each of these changes is characterized by the occurrence of continuous activity that is inefficient and diffused. The signal/noise ratio of several critical biological events is thus reduced as beneficial responses are gradually replaced by their impaired and deleterious variants.
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What OpenQuestion holds
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.