ReviewAging medicine (Milton (N.S.W))2022
Critical appraisal on mitochondrial dysfunction in Alzheimer's disease.
Review in Aging medicine (Milton (N.S.W)), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 20 citations in OpenAlex.
- E3 Ubiquitin Ligase Nedd4-2 Exacerbates Seizure-Induced Mitochondrial Defects in an Alzheimer's Disease Mouse Model.Journal of neurochemistry · 2026Article
- Heterotrimetallic Au@CuMaterials today. Bio · 2026Article
- L-Theanine Prolongs the Lifespan by Activating Multiple Molecular Pathways in Ultraviolet C-ExposedMolecules (Basel, Switzerland) · 2024Article
- Article
- Identification of potential neuroprotective compound fromAging medicine (Milton (N.S.W)) · 2023Article
- Review
- Plausible Role of Stem Cell Types for Treating and Understanding the Pathophysiology of Depression.Pharmaceutics · 2023Review
- Review
- Critical appraisal on mitochondrial dysfunction in Alzheimer's disease.Aging medicine (Milton (N.S.W)) · 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is widely recognized that Alzheimer's disease (AD) is a common type of progressive neurodegenerative disorder that results in cognitive impairment over time. Approximately 152 million cases of AD are predicted to be reported by 2050. Amyloid plaques and tau proteins are two major hallmarks of AD which can be seen under electron microscope. Mitochondria plays a vital role in the pathogenesis of AD and mitochondria disruption leads to mitochondrial DNA (mtDNA) dysfunction, alteration of mitochondria dependent Ca2+ homeostasis, copper dysfunction, immune cell dysfunction, etc. In this review, we try to cover all the mechanisms related with mitochondrial dysfunction and mitochondrial pathogenesis that may help us to better understand AD as well as open a new era for therapeutic target of AD and treat this progressive disease.
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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.