ReviewInternational journal of molecular sciences2021
ATP Synthase and Mitochondrial Bioenergetics Dysfunction in Alzheimer's Disease.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 64 citations in OpenAlex.
- Mitochondria-Targeted Nanotherapies in Aging Neurodegenerative Disorders: Emerging Prospects and Clinical Potential.Advanced healthcare materials · 2026Review
- From Food Additives to Neurodegeneration: The Emerging Role of Polyphosphates in Tauopathies.ACS chemical neuroscience · 2026Review
- Three-dimensional interactive network: Mitochondrial-metabolic-calcium homeostasis driving Alzheimer's disease.Genes & diseases · 2026Review
- From Lipids to Mitochondria: Shared Metabolic Alterations in Obesity and Alzheimer's Disease.Cells · 2026Review
- Direct energy consumption by inhibitory GABAFrontiers in neuroscience · 2026Article
- Article
- Integrating simulated and experimental data to identify mitochondrial bioenergetic defects in Parkinson's Disease models.PloS one · 2026Article
- Neuroprotective Effect of Marine-Derived Nacre Extract against Aβ-Induced Toxicity via Preservation of Mitochondrial Function and Biogenesis.Neurochemical research · 2025Article
- Article
- Disturbances in Mitochondrial Network, Biogenesis, and Mitochondria-Mediated Inflammatory Responses in Selected Brain Structures of Rats Exposed to Lead (Pb) During Prenatal and Neonatal Development.International journal of molecular sciences · 2025Article
- Integrative multi-omics analysis of autism spectrum disorder reveals unique microbial macromolecules interactions.Journal of advanced research · 2025Article
- Effects of nutrients and diet on mitochondrial dysfunction: An opportunity for therapeutic approaches in human disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Improvement in Insulin Sensitivity Prevents Decline in Glucose Uptake, Functional Connectivity, and Volume in the Insulin Resistant Human Brain.Research square · 2025Article
- Inorganic Polyphosphate: An Emerging Regulator of Neuronal Bioenergetics and Its Implications in Neuroprotection.Biomolecules · 2025Review
- Role of Mitochondrial Dysfunctions in Neurodegenerative Disorders: Advances in Mitochondrial Biology.Molecular neurobiology · 2025Review
- Mitochondrial Dysfunction as a Pathogenesis and Therapeutic Strategy for Metabolic-Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2025Review
- Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Gene Co-Expression Analysis Reveals Functional Differences Between Early- and Late-Onset Alzheimer's Disease.Current issues in molecular biology · 2025Article
- Resisting decline: the neuroprotective role of resistance exercise in supporting cerebrovascular function and brain health in aging.Frontiers in physiology · 2025Review
- Key Proteins in Rat Cerebral Cortex: Application ofMolecules (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's Disease (AD) is the most common neurodegenerative disorder in our society, as the population ages, its incidence is expected to increase in the coming decades. The etiopathology of this disease still remains largely unclear, probably because of the highly complex and multifactorial nature of AD. However, the presence of mitochondrial dysfunction has been broadly described in AD neurons and other cellular populations within the brain, in a wide variety of models and organisms, including post-mortem humans. Mitochondria are complex organelles that play a crucial role in a wide range of cellular processes, including bioenergetics. In fact, in mammals, including humans, the main source of cellular ATP is the oxidative phosphorylation (OXPHOS), a process that occurs in the mitochondrial electron transfer chain (ETC). The last enzyme of the ETC, and therefore the ulterior generator of ATP, is the ATP synthase. Interestingly, in mammalian cells, the ATP synthase can also degrade ATP under certain conditions (ATPase), which further illustrates the crucial role of this enzyme in the regulation of cellular bioenergetics and metabolism. In this collaborative review, we aim to summarize the knowledge of the presence of dysregulated ATP synthase, and of other components of mammalian mitochondrial bioenergetics, as an early event in AD. This dysregulation can act as a trigger of the dysfunction of the organelle, which is a clear component in the etiopathology of AD. Consequently, the pharmacological modulation of the ATP synthase could be a potential strategy to prevent mitochondrial dysfunction in AD.
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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.