ReviewBiomedicines2022
Aβ and Tau Regulate Microglia Metabolism via Exosomes in Alzheimer's Disease.
Review in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 35 citations in OpenAlex.
- Exosomes in Alzheimer's Disease: From Pathological Mechanisms to Biomarker Potential and Therapeutic Applications.Molecular neurobiology · 2026Review
- PDE4A knockdown rescues alcohol-induced cognitive impairment and synaptic dysfunction via the cAMP/PKA/CREB pathway.The international journal of neuropsychopharmacology · 2026Article
- Cargo-driven extracellular vesicles as pharmaceutical nanocarriers: A pharmaceutics-oriented comparison of animal exosomes and plant-derived exosome-like nanoparticles.International journal of pharmaceutics: X · 2026Review
- Glycolysis: The Bridge Between Cellular Interaction and Alzheimer's Disease.Biomolecules · 2026Review
- Glucose metabolic reprogramming: mechanisms and therapeutic implications in neuroinflammation.Frontiers in immunology · 2026Review
- Glial lactate metabolism and transport in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Microglia-Neuron Interactions in Alzheimer's Disease.Current neuropharmacology · 2026Review
- miR-132 and Its Exosomal Form in Alzheimer's Disease: Linking Epigenetic Regulation to Neurodegeneration.Molecular neurobiology · 2025Review
- Exosomes as Emerging Therapeutic Platforms in Neurological and Psychiatric Disorders.Pharmaceutical medicine · 2025Review
- Understanding the role of microglia in Alzheimer's disease: insights into mechanisms, acupuncture, and potential therapeutic targets.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Review
- The Interplay Between Exosomes and Gut Microbiota in Neuroinflammation: A New Frontier in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Decoding microglial immunometabolism: a new frontier in Alzheimer's disease research.Molecular neurodegeneration · 2025Review
- ApoE3 R136S binds to Tau and blocks its propagation, suppressing neurodegeneration in mice with Alzheimer's disease.Neuron · 2025Article
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- New progress on the role and mechanism of tau protein in Alzheimer's disease and depression.Frontiers in neurology · 2025Review
- Zika virus induces monocyte recruitment in the immunocompetent adult brain driving chronic inflammation.Frontiers in immunology · 2025Article
- Neuroinflammation and nutrition in Alzheimer's disease.Frontiers in neurology · 2025Review
- Broadening Horizons: Exploring the Cathepsin Family as Therapeutic Targets for Alzheimer's Disease.Aging and disease · 2024Review
- MiR-184 Mediated the Expression of ZNF865 in Exosome to Promote Procession in the PD Model.Molecular neurobiology · 2024Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
One of the most striking hallmarks shared by various neurodegenerative diseases, including Alzheimer's disease (AD), is microglia-mediated neuroinflammation. The main pathological features of AD are extracellular amyloid-β (Aβ) plaques and intracellular tau-containing neurofibrillary tangles in the brain. Amyloid-β (Aβ) peptide and tau protein are the primary components of the plaques and tangles. The crosstalk between microglia and neurons helps maintain brain homeostasis, and the metabolic phenotype of microglia determines its polarizing phenotype. There are currently many research and development efforts to provide disease-modifying therapies for AD treatment. The main targets are Aβ and tau, but whether there is a causal relationship between neurodegenerative proteins, including Aβ oligomer and tau oligomer, and regulation of microglia metabolism in neuroinflammation is still controversial. Currently, the accumulation of Aβ and tau by exosomes or other means of propagation is proposed as a regulator in neurological disorders, leading to metabolic disorders of microglia that can play a key role in the regulation of immune cells. In this review, we propose that the accumulation of Aβ oligomer and tau oligomer can propagate to adjacent microglia through exosomes and change the neuroinflammatory microenvironment by microglia metabolic reprogramming. Clarifying the relationship between harmful proteins and microglia metabolism will help people to better understand the mechanism of crosstalk between neurons and microglia, and provide new ideas for the development of AD drugs.
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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.