ReviewMolecular neurobiology2017
A Mitocentric View of Alzheimer's Disease.
Review in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Pooled it
- Synthesis and biological evaluation of novel hydrazone derivatives for the treatment of Alzheimer's disease.RSC advances · 2025Article
- Brain structural alterations in young women with premature ovarian insufficiency: Implications for dementia risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Role of Tau Protein Hyperphosphorylation in Diabetic Retinal Neurodegeneration.Journal of ophthalmology · 2025Review
- Cyclin-dependent Kinase 5 and Neurodegenerative Diseases.Molecular neurobiology · 2024Review
- Mitochondrial alterations in fibroblasts from sporadic Alzheimer's disease (AD) patients correlate with AD-related clinical hallmarks.Acta neuropathologica communications · 2024Article
- Desloratadine alleviates ALS-like pathology in hSOD1Acta pharmacologica Sinica · 2024Article
- Article
- Article
- Genetically controlled mtDNA deletions prevent ROS damage by arresting oxidative phosphorylation.eLife · 2022Article
- Endoplasmic reticulum stress induces mitochondrial dysfunction but not mitochondrial unfolded protein response in SH-SY5Y cells.Molecular and cellular biochemistry · 2022Article
- Small-molecule drugs development for Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- Mitochondrially-Targeted Therapeutic Strategies for Alzheimer's Disease.Current Alzheimer research · 2021Review
- Downregulation of ATP6V1A Involved in Alzheimer's Disease via Synaptic Vesicle Cycle, Phagosome, and Oxidative Phosphorylation.Oxidative medicine and cellular longevity · 2021Article
- The Crosstalk Between Pathological Tau Phosphorylation and Mitochondrial Dysfunction as a Key to Understanding and Treating Alzheimer's Disease.Molecular neurobiology · 2020Review
- Tauopathy-associated tau modifications selectively impact neurodegeneration and mitophagy in a novel C. elegans single-copy transgenic model.Molecular neurodegeneration · 2020Article
- Ketotherapeutics for neurodegenerative diseases.International review of neurobiology · 2020Review
- Review
- The vexing complexity of the amyloidogenic pathway.Protein science : a publication of the Protein Society · 2019Review
- Small molecules as therapeutic drugs for Alzheimer's disease.Molecular and cellular neurosciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease with an increasing morbidity, mortality, and economic cost. Plaques formed by amyloid beta peptide (Aβ) and neurofibrillary tangles formed by microtubule-associated protein tau are two main characters of AD. Though previous studies have focused on Aβ and tau and got some progressions on their toxicity mechanisms, no significantly effective treatments targeting the Aβ and tau have been found. However, it is worth noting that mounting evidences showed that mitochondrial dysfunction is an early event during the process of AD pathologic changes. What is more, these studies also showed an obvious association between mitochondrial dysfunction and Aβ/tau toxicity. Furthermore, both genetic and environmental factors may increase the oxidative stress and the mitochondria are also the sensitive target of ROS, which may form a vicious feedback between mitochondrial dysfunction and oxidative stress, eventually resulting in deficient energy, synaptic failure, and cell death. This article reviews the previous related studies from different aspects and concludes the critical roles of mitochondrial dysfunction in AD, suggesting a different route to AD therapy, which may guide the research and treatment direction.
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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.