ReviewCell communication and signaling : CCS2021
Methylation as a key regulator of Tau aggregation and neuronal health in Alzheimer's disease.
Review in Cell communication and signaling : CCS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses 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.
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Who cites it
45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 87 citations in OpenAlex.
- Environmental epigenetic modifiers in neurodegenerative diseases: a systematic review of epigenomic mechanisms and therapeutic targets.Frontiers in epigenetics and epigenomics · 2026Pooled it
- Blood levels of circulating methionine components in Alzheimer's disease and mild cognitive impairment: A systematic review and meta-analysis.Frontiers in aging neuroscience · 2022Pooled it
- Deconfounded-Debiased Estimation and Inference for High-Dimensional Mediation Analysis With Pervasive Hidden Confounders.Statistics in medicine · 2026Article
- Advances in Alzheimer's disease: mechanistic insights and therapeutic targets.Science China. Life sciences · 2026Review
- Metal Binding to Tau Protein: Physiological and Pathological Relevance.Biochemistry · 2026Review
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Biophysical assessment of the molecular mechanisms of Tau aggregation and its role in Alzheimer's disease.Protein science : a publication of the Protein Society · 2026Review
- Post-translational modifications as a regulatory code for tau function in health and disease.Frontiers in dementia · 2026Review
- Lysine methylation is an endogenous post-translational modifications of tau protein in human brain and a modulator of aggregation propensity.Methods in enzymology · 2026Article
- Consensus statement on exploring the Nexus between nutrition, brain health and dementia prevention.Nutrition & metabolism · 2025Review
- The Role and Pathogenesis of Tau Protein in Alzheimer's Disease.Biomolecules · 2025Review
- Isoforms of Phosphorylated Tau as Potential Biomarkers for Alzheimer's Disease: The Contribution of Mass Spectrometry-Based Proteomics.NeuroSci · 2025Review
- Empagliflozin and memantine combination ameliorates cognitive impairment in scopolamine + heavy metal mixture-induced Alzheimer's disease in rats: role of AMPK/mTOR, BDNF, BACE-1, neuroinflammation, and oxidative stress.Inflammopharmacology · 2025Article
- Inhibition of SCFCommunications biology · 2025Article
- Uncovering the epigenetic regulatory clues of PRRT1 in Alzheimer's disease: a strategy integrating multi-omics analysis with explainable machine learning.Alzheimer's research & therapy · 2025Article
- New progress on the role and mechanism of tau protein in Alzheimer's disease and depression.Frontiers in neurology · 2025Review
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
- Exploration of Epigenetic Mechanisms and Biomarkers Among Patients with Very-Late-Onset Schizophrenia-Like Psychosis.Neuropsychiatric disease and treatment · 2025Article
- Post-translational modifications of proteins in cardiovascular diseases examined by proteomic approaches.The FEBS journal · 2025Review
- Targeting USP11 regulation by a novel lithium-organic coordination compound improves neuropathologies and cognitive functions in Alzheimer transgenic mice.EMBO molecular medicine · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neurodegenerative diseases like Alzheimer's, Parkinson's and Huntington's disease involves abnormal aggregation and accumulation of toxic proteins aggregates. Post-translational modifications (PTMs) of the causative proteins play an important role in the etiology of disease as they could either slow down or accelerate the disease progression. Alzheimer disease is associated with the aggregation and accumulation of two major protein aggregates-intracellular neurofibrillary tangles made up of microtubule-associated protein Tau and extracellular Amyloid-β plaques. Post-translational modifications are important for the regulation of Tau`s function but an imbalance in PTMs may lead to abnormal Tau function and aggregation. Tau methylation is one of the important PTM of Tau in its physiological state. However, the methylation signature on Tau lysine changes once it acquires pathological aggregated form. Tau methylation can compete with other PTMs such as acetylation and ubiquitination. The state of PTM at these sites determines the fate of Tau protein in terms of its function and stability. The global methylation in neurons, microglia and astrocytes are involved in multiple cellular functions involving their role in epigenetic regulation of gene expression via DNA methylation. Here, we have discussed the effect of methylation on Tau function in a site-specific manner and their cross-talk with other lysine modifications. We have also elaborated the role of methylation in epigenetic aspects and neurodegenerative conditions associated with the imbalance in methylation metabolism affecting global methylation state of cells. Video abstract.
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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.