SynthesisFunctional neurology
The possible involvement of mitochondrial dysfunctions in Lewy body dementia: a systematic review.
Synthesis in Functional neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Hippocampal transcriptome-wide association study and pathway analysis of mitochondrial solute carriers in Alzheimer's disease.Translational psychiatry · 2024Pooled it
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Association of mitochondrial genetic background with pS65-Ub in Lewy body disease.Acta neuropathologica · 2026Article
- Potential common pathogenesis of several neurodegenerative diseases.Neural regeneration research · 2026Article
- Molecular Crossroads: Shared and Divergent Molecular Signatures in Alzheimer's Disease and Dementia with Lewy Bodies.International journal of molecular sciences · 2025Review
- Mitochondrial protein import stress augments α-synuclein aggregation and neural damage independent of bioenergetics.Research square · 2025Article
- Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein.Molecular neurodegeneration · 2025Review
- The Unified Theory of Neurodegeneration Pathogenesis Based on Axon Deamidation.International journal of molecular sciences · 2025Review
- Mitochondria: great balls of fire.The FEBS journal · 2024Review
- Mitochondrial Inherited Disorders and their Correlation with Neurodegenerative Diseases.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Escalating Bi-Directional Feedback Loops between Proinflammatory Microglia and Mitochondria in Ageing and Post-Diagnosis of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Melanin: a unifying theory of disease as exemplified by Parkinson's, Alzheimer's, and Lewy body dementia.Frontiers in immunology · 2023Article
- Article
- The Protective Role of Neurogenetic Components in Reducing Stress-Related Effects during Spaceflights: Evidence from the Age-Related Positive Memory Approach.Life (Basel, Switzerland) · 2022Review
- Role of PITRM1 in Mitochondrial Dysfunction and Neurodegeneration.Biomedicines · 2021Review
- Mitophagy in Human Diseases.International journal of molecular sciences · 2021Review
- Small Non-coding RNAs: New Class of Biomarkers and Potential Therapeutic Targets in Neurodegenerative Disease.Frontiers in genetics · 2019Review
- Aβ exacerbates α-synuclein-induced neurotoxicity through impaired insulin signaling in α-synuclein-overexpressed human SK-N-MC neuronal cells.CNS neuroscience & therapeutics · 2018Article
- Ethnopharmacological Approaches for Dementia Therapy and Significance of Natural Products and Herbal Drugs.Frontiers in aging neuroscience · 2018Review
- MicroRNAs and Target Genes As Biomarkers for the Diagnosis of Early Onset of Parkinson Disease.Frontiers in molecular neuroscience · 2017Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hallmark of dementia with Lewy bodies (DLB) is the “Lewy body”, an abnormal aggregation of alpha-synuclein found in some areas of the brain. The brain is the organ/system that is most vulnerable to this oxidative damage, and reactive oxygen species can cause neurodegenerative diseases. Different models of mitochondrial deregulation have been compared in DLB. The results are consistent with the hypothesis that alpha-synuclein affects the mitochondria themselves, increasing their sensitivity or leading to cell death through protective (neurosin) and accelerating (cytochrome c) factors. This systematic review suggests that mitochondria play an important role in neurodegeneration and a crucial role in the formation of Lewy bodies. DLB is a disease characterized by abnormal accumulation of alpha-synuclein that could result in the release of cytochrome c and subsequent activation of the apoptotic cascade.
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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.