ReviewNeural regeneration research2023
Crosslink between mutations in mitochondrial genes and brain disorders: implications for mitochondrial-targeted therapeutic interventions.
Review in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Review
- Mitochondrial targeted antioxidants as potential therapy for huntington's disease.Pharmacological reports : PR · 2024Review
- Review
- Unraveling the nexus of age, epilepsy, and mitochondria: exploring the dynamics of cellular energy and excitability.Frontiers in pharmacology · 2024Review
- Mitochondria in Huntington's disease: implications in pathogenesis and mitochondrial-targeted therapeutic strategies.Neural regeneration research · 2023Review
- Redox Imbalance in Neurological Disorders in Adults and Children.Antioxidants (Basel, Switzerland) · 2023Review
- The Link between Oxidative Stress, Mitochondrial Dysfunction and Neuroinflammation in the Pathophysiology of Alzheimer's Disease: Therapeutic Implications and Future Perspectives.Antioxidants (Basel, Switzerland) · 2022Review
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
At the present, association of mitochondrial dysfunction and progression of neurological disorders has gained significant attention. Defects in mitochondrial network dynamics, point mutations, deletions, and interaction of pathogenomic proteins with mitochondria are some of the possible underlying mechanisms involved in these neurological disorders. Mitochondrial genetics, defects in mitochondrial oxidative phosphorylation machinery, and reactive oxygen species production might share common crosstalk in the progression of these neurological disorders. It is of significant interests to explore and develop therapeutic strategies aimed at correcting mitochondrial abnormalities. This review provided insights on mitochondrial dysfunction/mutations involved in the progression of Alzheimer's disease, Huntington's disease, and epilepsy with a special focus on Parkinson's disease pathology. Along with the deleterious effects of mitochondrial mutations in aforesaid neurological disorders, this paper unraveled the available therapeutic strategy, specifically aiming to improve mitochondrial dysfunction, drugs targeting mitochondrial proteins, gene therapies aimed at correcting mutant mtDNA, peptide-based approaches, and lipophilic cations.
Indexed as
Identifiers
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.