ReviewNeural regeneration research2018
Modulation of mitochondrial bioenergetics as a therapeutic strategy in Alzheimer's disease.
Review in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Mitochondrial dysfunction, oxidative stress, neuroinflammation, and metabolic alterations in the progression of Alzheimer's disease: A meta-analysis of in vivo magnetic resonance spectroscopy studies.Ageing research reviews · 2021Pooled it
- Redox therapy for neuropsychiatric disorders: Molecular mechanisms and biomarker development.Science advances · 2026Review
- Naringin and Naringenin: Potential Multi-Target Agents for Alzheimer's Disease.Current medical science · 2024Review
- Sera from people with HIV and depression induce commensurate metabolic alterations in astrocytes: toward precision diagnoses and therapies.NeuroImmune pharmacology and therapeutics · 2024Article
- Mitochondrial dysfunction and therapeutic perspectives in osteoporosis.Frontiers in endocrinology · 2024Review
- Regenerative medicine improve neurodegenerative diseases.Cell and tissue banking · 2023Review
- Mitochondrial Transfer as a Novel Therapeutic Approach in Disease Diagnosis and Treatment.International journal of molecular sciences · 2023Review
- The Role of Mitochondrial Dysfunction in Alzheimer's: Molecular Defects and Mitophagy-Enhancing Approaches.Life (Basel, Switzerland) · 2023Review
- Mitochondrial CaBiomedicines · 2022Review
- Therapeutic Potential of Targeting Mitochondria for Alzheimer's Disease Treatment.Journal of clinical medicine · 2022Review
- Targeting mitochondrial bioenergetics as a promising therapeutic strategy in metabolic and neurodegenerative diseases.Biomedical journal · 2022Review
- Article
- Caloric Restriction Mimetic 2-Deoxyglucose Reduces Inflammatory Signaling in Human Astrocytes: Implications for Therapeutic Strategies Targeting Neurodegenerative Diseases.Brain sciences · 2022Article
- Proteolysis targeting chimera technology: a novel strategy for treating diseases of the central nervous system.Neural regeneration research · 2021Review
- Naringin Exhibits Mas Receptor-Mediated Neuroprotection Against Amyloid Beta-Induced Cognitive Deficits and Mitochondrial Toxicity in Rat Brain.Neurotoxicity research · 2021Article
- Roles of PRR-Mediated Signaling Pathways in the Regulation of Oxidative Stress and Inflammatory Diseases.International journal of molecular sciences · 2021Review
- Stem cell-derived mitochondria transplantation: A promising therapy for mitochondrial encephalomyopathy.CNS neuroscience & therapeutics · 2021Review
- Tetrahydroxystilbene glucoside protects against sodium azide-induced mitochondrial dysfunction in human neuroblastoma cells.Chinese herbal medicines · 2021Article
- The Potential Benefits of Nanotechnology in Treating Alzheimer's Disease.BioMed research international · 2021Review
- Targeting Age-Related Neurodegenerative Diseases by AAV-Mediated Gene Therapy.Advances in experimental medicine and biology · 2021Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is an increasingly pressing worldwide public-health, social, political and economic concern. Despite significant investment in multiple traditional therapeutic strategies that have achieved success in preclinical models addressing the pathological hallmarks of the disease, these efforts have not translated into any effective disease-modifying therapies. This could be because interventions are being tested too late in the disease process. While existing therapies provide symptomatic and clinical benefit, they do not fully address the molecular abnormalities that occur in AD neurons. The pathophysiology of AD is complex; mitochondrial bioenergetic deficits and brain hypometabolism coupled with increased mitochondrial oxidative stress are antecedent and potentially play a causal role in the disease pathogenesis. Dysfunctional mitochondria accumulate from the combination of impaired mitophagy, which can also induce injurious inflammatory responses, and inadequate neuronal mitochondrial biogenesis. Altering the metabolic capacity of the brain by modulating/potentiating its mitochondrial bioenergetics may be a strategy for disease prevention and treatment. We present insights into the mechanisms of mitochondrial dysfunction in AD brain as well as an overview of emerging treatments with the potential to prevent, delay or reverse the neurodegenerative process by targeting mitochondria.
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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.