ArticleJournal of Alzheimer's disease : JAD2010
MAPT isoforms: differential transcriptional profiles related to 3R and 4R splice variants.
Article in Journal of Alzheimer's disease : JAD, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 72 citations in OpenAlex.
- Patient-derived forebrain cortical organoids reveal biphasic tau-MAP6-microtubule axis dysfunction in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- RNArchitects: how hnRNPs shape neuronal landscapes.Brain : a journal of neurology · 2026Review
- Comparing Gallyas and AT8 staining for quantification of tau pathology in subregions of the human hippocampus.Journal of neuropathology and experimental neurology · 2026Article
- NRF2 deficit prevents pathologic Tau seeding and spreading in an induced tauopathy mouse model.Redox biology · 2026Article
- Distinct tau filament folds in familial frontotemporal dementia due to thebioRxiv : the preprint server for biology · 2026Article
- Toward common treatment strategies: convergent proteinopathies and mitochondrial dysfunction in Alzheimer's and Parkinson's diseases.Frontiers in neuroscience · 2026Review
- Tau protein: Physiological functions and multifaceted roles in neurodegenerative and psychiatric disorders.Genomic psychiatry : advancing science from genes to society · 2025Article
- A high-throughput drug screening assay for anti-tau aggregation using split GFP and flow cytometry.Scientific reports · 2025Article
- In Vitro Evaluation of Amide-Linked Coumarin Scaffolds for the Inhibition of α‑Synuclein and Tau Aggregation.ACS omega · 2025Article
- Herpes simplex virus-1 infection alters microtubule-associated protein Tau splicing and promotes Tau pathology in neural models of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- Spliceosome protein alterations differentiate hubs of the default mode connectome during the progression of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- Decoding tau acetylation in Alzheimer's disease and tauopathies: from site-specific mechanisms to therapeutic horizons.BMB reports · 2025Review
- U1-70K and U1A and tau pathogenesis in demented and non-demented individuals with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Rational Modulation of Liquid-Liquid Phase Separation Offers Novel Ways to Combat Tauopathies.International journal of molecular sciences · 2025Review
- Development of MAPT S305 mutation human iPSC lines exhibiting elevated 4R tau expression and functional alterations in neurons and astrocytes.Cell reports · 2024Article
- Cellular and pathological functions of tau.Nature reviews. Molecular cell biology · 2024Review
- Pathological and physiological functional cross-talks of α-synuclein and tau in the central nervous system.Neural regeneration research · 2024Review
- Ensemble-based design of tau to inhibit aggregation while preserving biological activity.Research square · 2024Article
- Untangling Tau: Molecular Insights into Neuroinflammation, Pathophysiology, and Emerging Immunotherapies.Current issues in molecular biology · 2023Review
- Patients carrying the mutation p.R406W in MAPT present with non-conforming phenotypic spectrum.Brain : a journal of neurology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Tau aggregation in neurofibrillary tangles is a pathological hallmark in tauopathies including Alzheimer's disease (AD). The predominant aggregation of certain MAPT (tau gene) isoforms, either the 4-repeat (4R tau) or the 3-repeat (3R tau) isoform has been widely described in tauopathies. Alterations of the 4R tau to 3R tau ratio may be a key for tau-related neurodegeneration. To study the biological consequences in expression between tau splicing isoforms 4R and 3R, we analyzed the main neurobiological effects of inclusion of the repeat region coded by exon 10 in MAPT. We compared the transcriptional profiles of the 4R tau isoforms to 3R tau isoforms using whole-genome gene expression profiling microarrays using human neuroblastoma SH-SY5Y cell lines overexpressing either human 4R tau or 3R tau isoforms. We identified 68 transcripts that differed significantly (at p < 0.001) between 4R and 3R isoforms as conditioned on a second variant, the so-called 2N inclusion. We extended these findings in a 2 × 2 ANOVA to examine interaction effects of these variants. Transcripts involved in embryonic development were downregulated when exon 10 was present, while transcripts related to outgrowth of neurites were generally upregulated. An important pathway implicated in AD also differed between the 3R and 4R cell lines, Wnt signaling. These studies demonstrate expression differences between MAPT isoforms 4R tau and 3R tau due to the inclusion/exclusion of the repeat region coded for by exon 10. Our data add to complex findings on the role of 3R/4R in normal and abnormal neuronal function and highlight several molecular mechanisms that might drive neurodegeneration, or perhaps, set the stage for it.
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