ReviewInternational journal of molecular sciences2021
Mitochondrial Dysfunction as a Driver of Cognitive Impairment in Alzheimer's Disease.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07651787 (Neurovascular and Mitochondrial Mechanisms of Transcranial Photobiomodulation in Vascular Mild Cognitive Impairment), which is not on this map. Cited by 130 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neurovascular and Mitochondrial Mechanisms of Transcranial Photobiomodulation in Vascular Mild Cognitive Impairment
Who cites it
130 citing papers in PubMed, 3 syntheses or guidelines pooled it, 213 citations in OpenAlex.
- Mitotherapy in Alzheimer's and Parkinson's diseases: A systematic review of preclinical studies.BMC neurology · 2025Pooled it
- A systematic review of the therapeutic potential of nicotinamide adenine dinucleotide precursors for cognitive diseases in preclinical rodent models.BMC neuroscience · 2025Pooled it
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- Beta 2-adrenergic pathway combats Alzheimer's disease: Restoring cognition and synaptic integrity.Neural regeneration research · 2026Article
- AI-based characterization of Alzheimer's disease phenotypes from population-scale single-cell data.Nature medicine · 2026Article
- Digital Cognitive Testing in Mitochondrial Disease: Validity and Challenges for Clinical Trial Use.Annals of clinical and translational neurology · 2026Article
- Interplay between brain-specific microRNAs and Alzheimer's disease.Neural regeneration research · 2026Article
- Advances in the Core Role and Mechanisms of Mitochondrial Dysfunction in Alzheimer's Disease.Brain and behavior · 2026Review
- Review
- Beyond energy production: targeting mitochondrial biogenesis in aging and cancer with phytochemical intervention.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Mitochondrial dysfunction in sleep deprivation.Metabolic brain disease · 2026Review
- Article
- Mechanistic insights and therapeutic interventions of mitochondrial quality control in chemotherapy-related cognitive impairment.Neoplasia (New York, N.Y.) · 2026Review
- Targeting oxidative stress and neurodegeneration: the role of Putranjiva roxburghii in Alzheimer's.Inflammopharmacology · 2026Review
- Metabolic reprogramming of neurons in alzheimer disease: a biochemical perspective.Metabolic brain disease · 2026Review
- Misfolded Proteins and Cognitive Decline: Mechanistic Insights into Neurodegenerative Disorders.Neurology international · 2026Review
- Taurine as an Early-Phase Disease-Modifying Candidate for Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Article
- Synaptic aging and neurodegeneration: the role of synaptic vesicle dynamics and neurotransmitter imbalance.Biogerontology · 2026Review
- Expanding the cognitive spectrum of mitochondrial diseases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
70 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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most frequent cause of age-related neurodegeneration and cognitive impairment, and there are currently no broadly effective therapies. The underlying pathogenesis is complex, but a growing body of evidence implicates mitochondrial dysfunction as a common pathomechanism involved in many of the hallmark features of the AD brain, such as formation of amyloid-beta (Aβ) aggregates (amyloid plaques), neurofibrillary tangles, cholinergic system dysfunction, impaired synaptic transmission and plasticity, oxidative stress, and neuroinflammation, that lead to neurodegeneration and cognitive dysfunction. Indeed, mitochondrial dysfunction concomitant with progressive accumulation of mitochondrial Aβ is an early event in AD pathogenesis. Healthy mitochondria are critical for providing sufficient energy to maintain endogenous neuroprotective and reparative mechanisms, while disturbances in mitochondrial function, motility, fission, and fusion lead to neuronal malfunction and degeneration associated with excess free radical production and reduced intracellular calcium buffering. In addition, mitochondrial dysfunction can contribute to amyloid-β precursor protein (APP) expression and misprocessing to produce pathogenic fragments (e.g., Aβ1-40). Given this background, we present an overview of the importance of mitochondria for maintenance of neuronal function and how mitochondrial dysfunction acts as a driver of cognitive impairment in AD. Additionally, we provide a brief summary of possible treatments targeting mitochondrial dysfunction as therapeutic approaches for AD.
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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.