ReviewBrain pathology (Zurich, Switzerland)2016
Alzheimer's Disease: From Mitochondrial Perturbations to Mitochondrial Medicine.
Review in Brain pathology (Zurich, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
- Alkaloids from Dendrobium Nobile Lindl Improves Mitochondrial Function by Enhancing the Activity of v-ATPase in APP/PS1 Mice.Neurochemical research · 2026Article
- Therapeutic potential of melatonin-induced mitophagy in the pathogenesis of Alzheimer's disease.Inflammopharmacology · 2025Review
- Review
- Integrative bioinformatic approach reveals novel melatonin-related biomarkers for Alzheimer's disease.Scientific reports · 2025Article
- The multifaceted role of mitochondria in autism spectrum disorder.Molecular psychiatry · 2025Review
- Dual GSK3β/SIRT1 modulators for Alzheimer's: mechanisms, drug discovery and future perspectives.Frontiers in pharmacology · 2025Review
- Glucose Metabolic Abnormality: A Crosstalk between Depression and Alzheimer's Disease.Current neuropharmacology · 2025Review
- Gut microbiota-host lipid crosstalk in Alzheimer's disease: implications for disease progression and therapeutics.Molecular neurodegeneration · 2024Review
- Ligustilide-loaded liposome ameliorates mitochondrial impairments and improves cognitive function via the PKA/AKAP1 signaling pathway in a mouse model of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Article
- CoQAntioxidants (Basel, Switzerland) · 2024Review
- Mitochondria in Alzheimer's Disease Pathogenesis.Life (Basel, Switzerland) · 2024Review
- Review
- Chronic Cerebral Hypoperfusion-Induced Disturbed Proteostasis of Mitochondria and MAM Is Reflected in the CSF of Rats by Proteomic Analysis.Molecular neurobiology · 2023Article
- Dendrimers and Derivatives as Multifunctional Nanotherapeutics for Alzheimer's Disease.Pharmaceutics · 2023Review
- Mitoferrin-1 Promotes Proliferation and Abrogates Protein Oxidation via the Glutathione Pathway in Glioblastoma.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- The mechanism and efficacy of GLP-1 receptor agonists in the treatment of Alzheimer's disease.Frontiers in endocrinology · 2022Review
- Hippocampal disruptions of synaptic and astrocyte metabolism are primary events of early amyloid pathology in the 5xFAD mouse model of Alzheimer's disease.Cell death & disease · 2021Article
- Mitochondrial links between brain aging and Alzheimer's disease.Translational neurodegeneration · 2021Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related neurodegenerative diseases such as Alzheimer's disease (AD) are distressing conditions causing countless levels of suffering for which treatment is often insufficient or inexistent. Considered to be the most common cause of dementia and an incurable, progressive neurodegenerative disorder, the intricate pathogenic mechanisms of AD continue to be revealed and, consequently, an effective treatment needs to be developed. Among the diverse hypothesis that have been proposed to explain AD pathogenesis, the one concerning mitochondrial dysfunction has raised as one of the most discussed with an actual acceptance in the field. It posits that manipulating mitochondrial function and understanding the deficits that result in mitochondrial injury may help to control and/or limit the development of AD. To achieve such goal, the concept of mitochondrial medicine places itself as a promising gathering of strategies to directly manage the major insidious disturbances of mitochondrial homeostasis as well as attempts to directly or indirectly manage its consequences in the context of AD. The aim of this review is to summarize the evolution that occurred from the establishment of mitochondrial homeostasis perturbation as masterpieces in AD pathogenesis up until the development of mitochondrial medicine. Following a brief glimpse in the past and current hypothesis regarding the triad of aging, mitochondria and AD, this manuscript will address the major mechanisms currently believed to participate in above mentioned events. Both pharmacological and lifestyle interventions will also be reviewed as AD-related mitochondrial therapeutics.
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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.