ArticleBrain pathology (Zurich, Switzerland)2022
An early proinflammatory transcriptional response to tau pathology is age-specific and foreshadows reduced tau burden.
Article in Brain pathology (Zurich, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Neocortical tau propagation is a mediator of clinical heterogeneity in Alzheimer's disease.Molecular psychiatry · 2025Article
- Cystatin F-a key player in central nervous system disease.Journal of neuroinflammation · 2025Review
- Inpp5d haplodeficiency alleviates tau pathology in the PS19 mouse model of Tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Article
- Trichostatin A relieves anxiety-and depression-like symptoms in APP/PS1 mice.Frontiers in pharmacology · 2024Article
- Tau seeding and spreading in vivo is supported by both AD-derived fibrillar and oligomeric tau.Acta neuropathologica · 2023Article
- An early proinflammatory transcriptional response to tau pathology is age-specific and foreshadows reduced tau burden.Brain pathology (Zurich, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age is one of the strongest risk factors for the development of neurodegenerative diseases, the majority of which involve misfolded protein aggregates in the brain. These protein aggregates are thought to drive pathology and are attractive targets for the development of new therapies. However, it is unclear how age influences the onset of pathology and the accompanying molecular response. To address this knowledge gap, we used a model of seeded tau pathology to profile the transcriptomic changes in 3 and 12 month old mice in response to developing tau hyperphosphorylation and aggregation. First, we found the burden of hyperphosphorylated tau pathology in mice injected at 12 months of age was moderately reduced compared to animals injected at 3 months. On a molecular level, we found an inflammation-related subset of genes, including C3 and the disease-associated microglia genes Ctsd, Cst7, and Clec7a, were more expressed early in disease in 12 but not 3 month old mice. These findings provide evidence of an early, age-specific response to tau pathology, which could serve as a marker for the severity of downstream pathology.
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