ArticleActa neuropathologica communications2021
Tau isoforms are differentially expressed across the hippocampus in chronic traumatic encephalopathy and Alzheimer's disease.
Article in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Neuropathology in chronic traumatic encephalopathy: a systematic review of comparative post-mortem histology literature.Acta neuropathologica communications · 2022Pooled it
- Dynamic [Molecular neurodegeneration · 2026Article
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- Divergent recovery trajectories after mild traumatic brain injury are characterized by distinct acute profiles of neurofilament light, 4R-tau, and white matter diffusivity.Journal of neurology · 2026Article
- CELF2 promotes 4R Tau splicing via nuclear clustering and drives cognitive dysfunction in tauopathy models.Nature communications · 2026Article
- Nitric oxide drives proteomic diversity through alternative splicing.Molecular cell · 2026Article
- Advancing biomarker development for chronic traumatic encephalopathy: Summary and recommendations from the 2025 Leon Thal Summit.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Connecting HTT intermediate alleles and microRNA dysregulation to enhanced tauopathy in late-onset Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- CELF2 Promotes Tau Exon 10 Inclusion via Hinge Domain-Mediated Nuclear Condensation, Driving Cognitive Dysfunction in Tauopathy Models.Research square · 2026Article
- Spilling the T: T cells in tauopathy mechanisms, disease progression, and therapeutic horizons.Molecular neurodegeneration advances · 2026Review
- Toward nanomedicine-enabled RNA therapeutics for Alzheimer's disease.Molecular neurodegeneration advances · 2026Review
- Neocortical tau propagation is a mediator of clinical heterogeneity in Alzheimer's disease.Molecular psychiatry · 2025Article
- Tau filaments with the Alzheimer fold in human MAPT mutants V337M and R406W.Nature structural & molecular biology · 2025Article
- Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.Molecular neurodegeneration · 2025Review
- High-dimensional proteomic analysis for pathophysiological classification of traumatic brain injury.Brain : a journal of neurology · 2025Article
- Calcineurin inhibition may prevent Alzheimer disease in people with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Article
- Perivascular glial reactivity is a feature of phosphorylated tau lesions in chronic traumatic encephalopathy.Acta neuropathologica · 2025Article
- Functional classification of tauopathy strains reveals the role of protofilament core residues.Science advances · 2025Article
- A mouse model of early sporadic tau pathology induces neurogenic plasticity in the hippocampus.PloS one · 2025Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease, characterized by hyperphosphorylated tau, found in individuals with a history of exposure to repetitive head impacts. While the neuropathologic hallmark of CTE is found in the cortex, hippocampal tau has proven to be an important neuropathologic feature to examine the extent of disease severity. However, the hippocampus is also heavily affected in many other tauopathies, such as Alzheimer's disease (AD). How CTE and AD differentially affect the hippocampus is unclear. Using immunofluorescent analysis, a detailed histologic characterization of 3R and 4R tau isoforms and their differential accumulation in the temporal cortex in CTE and AD was performed. CTE and AD were both observed to contain mixed 3R and 4R tau isoforms, with 4R predominating in mild disease and 3R increasing proportionally as pathological severity increased. CTE demonstrated high levels of tau in hippocampal subfields CA2 and CA3 compared to CA1. There were also low levels of tau in the subiculum compared to CA1 in CTE. In contrast, AD had higher levels of tau in CA1 and subiculum compared to CA2/3. Direct comparison of the tau burden between AD and CTE demonstrated that CTE had higher tau densities in CA4 and CA2/3, while AD had elevated tau in the subiculum. Amyloid beta pathology did not contribute to tau isoform levels. Finally, it was demonstrated that higher levels of 3R tau correlated to more severe extracellular tau (ghost tangles) pathology. These findings suggest that mixed 3R/4R tauopathies begin as 4R predominant then transition to 3R predominant as pathological severity increases and ghost tangles develop. Overall, this work demonstrates that the relative deposition of tau isoforms among hippocampal subfields can aid in differential diagnosis of AD and CTE, and might help improve specificity of biomarkers for in vivo diagnosis.
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