ReviewInternational journal of molecular sciences2018
Neuroimmune Tau Mechanisms: Their Role in the Progression of Neuronal Degeneration.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Long Non-coding RNA: Insight Into Mechanisms of Alzheimer's Disease.Frontiers in molecular neuroscience · 2021Pooled it
- Uncovering the intricacies of IGF-1 in Alzheimer's disease: new insights from regulation to therapeutic targeting.Inflammopharmacology · 2025Review
- Emerging role of gut microbiota extracellular vesicle in neurodegenerative disorders and insights on their therapeutic management.iMetaOmics · 2024Review
- Exploring the effect of gut microbiome on Alzheimer's disease.Biochemistry and biophysics reports · 2024Review
- The Therapeutic Potential ofBiology · 2024Article
- Immunoproteasome Subunit Low Molecular Mass Peptide 2 (LMP2) Deficiency Ameliorates LPS/AβMolecular neurobiology · 2024Article
- Isolation, Identification, Activity Evaluation, and Mechanism of Action of Neuroprotective Peptides from Walnuts: A Review.Nutrients · 2023Review
- Emerging Roles of Cells and Molecules of Innate Immunity in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Exercise suppresses neuroinflammation for alleviating Alzheimer's disease.Journal of neuroinflammation · 2023Review
- Alzheimer's Disease: An Updated Overview of Its Genetics.International journal of molecular sciences · 2023Review
- Review
- Neuroinflammation and Neuropathology.Neuroscience and behavioral physiology · 2022Article
- The neuroprotective effects of glucagon-like peptide 1 in Alzheimer's and Parkinson's disease: An in-depth review.Frontiers in neuroscience · 2022Review
- A Negative Energy Balance Is Associated with Metabolic Dysfunctions in the Hypothalamus of a Humanized Preclinical Model of Alzheimer's Disease, the 5XFAD Mouse.International journal of molecular sciences · 2021Article
- The Microbiota-Gut-Brain Axis and Alzheimer's Disease: Neuroinflammation Is to Blame?Nutrients · 2020Review
- The Role of Natural Compounds and their Nanocarriers in the Treatment of CNS Inflammation.Biomolecules · 2020Review
- Acylated Ghrelin as a Multi-Targeted Therapy for Alzheimer's and Parkinson's Disease.Frontiers in neuroscience · 2020Review
- Increasing Tau 4R Tau Levels Exacerbates Hippocampal Tau Hyperphosphorylation in the hTau Model of Tauopathy but Also Tau Dephosphorylation Following Acute Systemic Inflammation.Frontiers in immunology · 2020Article
- Neuroinflammation as a Common Feature of Neurodegenerative Disorders.Frontiers in pharmacology · 2019Review
- Tocotrienol Rich Fraction Supplementation Modulate Brain Hippocampal Gene Expression in APPswe/PS1dE9 Alzheimer's Disease Mouse Model.Journal of Alzheimer's disease : JAD · 2019Article
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
Progressive neurodegenerative pathologies in aged populations are an issue of major concern worldwide. The microtubule-associated protein tau is able to self-aggregate to form abnormal supramolecular structures that include small oligomers up to complex polymers. Tauopathies correspond to a group of diseases that share tau pathology as a common etiological agent. Since microglial cells play a preponderant role in innate immunity and are the main source of proinflammatory factors in the central nervous system (CNS), the alterations in the cross-talks between microglia and neuronal cells are the main focus of studies concerning the origins of tauopathies. According to evidence from a series of studies, these changes generate a feedback mechanism reactivating microglia and provoking constant cellular damage. Thus, the previously summarized mechanisms could explain the onset and progression of different tauopathies and their functional/behavioral effects, opening the window towards an understanding of the molecular basis of anomalous tau interactions. Despite clinical and pathological differences, increasing experimental evidence indicates an overlap between tauopathies and synucleinopathies, considering that neuroinflammatory events are involved and the existence of protein misfolding. Neurofibrillary tangles of pathological tau (NFT) and Lewy bodies appear to coexist in certain brain areas. Thus, the co-occurrence of synucleinopathies with tauopathies is evidenced by several investigations, in which NFT were found in the substantia nigra of patients with Parkinson's disease, suggesting that the pathologies share some common features at the level of neuroinflammatory events.
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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.