ArticleActa neuropathologica communications2019
Enhanced phosphorylation of T153 in soluble tau is a defining biochemical feature of the A152T tau risk variant.
Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Tau A152T risk variant drives distinct cell type transcriptional signatures in AD and PSP.Acta neuropathologica · 2026Article
- Amyloid exacerbates tau and alpha-synuclein pathologies, behavioral impairments, and neuroinflammation in a mixed dementia model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Evaluating MAPT p.A152T as a risk factor for the 3R tauopathy Pick's disease.Brain communications · 2026Article
- Revolution of AAV in Drug Discovery: From Delivery System to Clinical Application.Journal of medical virology · 2025Review
- Article
- Profiling the impact of different tau species on glial cell biology.Frontiers in cell and developmental biology · 2025Article
- Toward an animal model of Progressive Supranuclear Palsy.Frontiers in neuroscience · 2024Review
- Network analysis identifies strain-dependent response to tau and tau seeding-associated genes.The Journal of experimental medicine · 2023Article
- High-content image-based analysis and proteomic profiling identifies Tau phosphorylation inhibitors in a human iPSC-derived glutamatergic neuronal model of tauopathy.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Pathogenic mutations in the tau gene (microtubule associated protein tau, MAPT) are linked to the onset of tauopathy, but the A152T variant is unique in acting as a risk factor for a range of disorders including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and dementia with Lewy bodies (DLB). In order to provide insight into the mechanism by which A152T modulates disease risk, we developed a novel mouse model utilizing somatic brain transgenesis with adeno-associated virus (AAV) to drive tau expression in vivo, and validated the model by confirming the distinct biochemical features of A152T tau in postmortem brain tissue from human carriers. Specifically, Tau
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