ReviewDrugs & aging2010
Mitochondrial dynamics in Alzheimer's disease: opportunities for future treatment strategies.
Review in Drugs & aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Protective Effects of Nicotinamide Adenine Dinucleotide and Related Precursors in Alzheimer's Disease: A Systematic Review of Preclinical Studies.Journal of molecular neuroscience : MN · 2021Pooled it
- Super-resolution Spinning-Disk Confocal Microscopy Using Optical Photon Reassignment (SoRa).Methods in molecular biology (Clifton, N.J.) · 2026Article
- Mapping key mitochondrial genes in Alzheimer's disease through human tissue and iPSC derived neurons.Scientific reports · 2025Article
- Potential Role of Membrane Contact Sites in the Dysregulation of the Crosstalk Between Mitochondria and Lysosomes in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Estimating progression of Alzheimer's disease with extracellular vesicle-related multi-omics risk models.Frontiers in aging neuroscience · 2025Article
- Diastolic dysfunction in Alzheimer's disease model mice is associated with Aβ-amyloid aggregate formation and mitochondrial dysfunction.Scientific reports · 2024Article
- Mitochondria in Alzheimer's Disease Pathogenesis.Life (Basel, Switzerland) · 2024Review
- Potential Retinal Biomarkers in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Mitochondrial Dysfunction Links to Impaired Hippocampal Serotonin Release in a Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- Therapeutic non-invasive brain treatments in Alzheimer's disease: recent advances and challenges.Inflammation and regeneration · 2022Review
- A Role for PGC-1a in the Control of Abnormal Mitochondrial Dynamics in Alzheimer's Disease.Cells · 2022Article
- Mechanisms of Mitochondrial Malfunction in Alzheimer's Disease: New Therapeutic Hope.Oxidative medicine and cellular longevity · 2022Review
- Alzheimer's disease and type 2 diabetes mellitus: Pathophysiologic and pharmacotherapeutics links.World journal of diabetes · 2021Review
- Mitochondrial ubiquitin ligase alleviates Alzheimer's disease pathology via blocking the toxic amyloid-β oligomer generation.Communications biology · 2021Article
- Exercise-Induced Benefits for Alzheimer's Disease by Stimulating Mitophagy and Improving Mitochondrial Function.Frontiers in aging neuroscience · 2021Review
- Changes in PGC-1α/SIRT1 Signaling Impact on Mitochondrial Homeostasis in Amyloid-Beta Peptide Toxicity Model.Frontiers in pharmacology · 2020Article
- Impact of Tau on Neurovascular Pathology in Alzheimer's Disease.Frontiers in neurology · 2020Review
- On the central role of mitochondria dysfunction and oxidative stress in Alzheimer's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019Review
- A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease.Cell death & disease · 2018Review
- Modulation of Mitochondrial Dynamics in Neurodegenerative Diseases: An Insight Into Prion Diseases.Frontiers in aging neuroscience · 2018Review
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 1 country.
Funding
Abstract
The complexities that underlie the cognitive impairment and neurodegeneration characteristic of Alzheimer's disease (AD) have yet to be completely understood, although many factors in disease pathogenesis have been identified. Particularly important in disease development seem to be mitochondrial disturbances. As pivotal role players in cellular metabolism, mitochondria are pertinent to cell survival and thus any deviation from their operation is certainly fatal. In this review, we describe how the dynamic balance of mitochondrial fission and fusion in particular is a necessary aspect of cell proliferation and that, as the cell ages, such balance is inevitably compromised to yield a destructive environment in which the cell cannot exist. Evidence for such disturbance is abundant in AD. Specifically, the dynamic balance of fission and fusion in AD is greatly shifted toward fission, and, as a result, affected neurons contain abnormal mitochondria that are unable to meet the metabolic demands of the cell. Moreover, mitochondrial distribution in AD cells is perinuclear, with few metabolic organelles in the distal processes, where they are normally distributed in healthy cells and are needed for exocytosis, ion channel pumps, synaptic function and other activities. AD neurons are thus characterized by increases in reactive oxidative species and decreases in metabolic capability, and, notably, these changes are evident very early in AD progression. We therefore believe that oxidative stress and altered mitochondrial dynamics contribute to the precipitation of AD pathology and thus cognitive decline. These implications provide a window for therapeutic intervention (i.e. mitochondrial protection) that has the potential to significantly deter AD progression if adequately developed. Current treatment strategies under investigation are described in this review.
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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.