ArticleCell death & disease2024
Glucocorticoid stress hormones stimulate vesicle-free Tau secretion and spreading in the brain.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Higher baseline CSF cortisol is associated with adverse 24-month tau-related, neuroimaging, and cognitive outcomes across the Alzheimer's disease continuum.European geriatric medicine · 2026Article
- Beyond microtubule regulation: the multifaceted roles of tau in neuronal function and dysfunction.Translational psychiatry · 2026Review
- APOE4 exacerbates glucocorticoid stress hormone-induced tau pathology via mitochondrial dysfunction.Cell death & disease · 2026Article
- From Early Adversity to Neurodegeneration: Stress Biomarkers as Predictive Signals for Lifespan Brain Health.International journal of molecular sciences · 2025Review
- Glucocorticoids regulate small extracellular vesicle (sEV) release via activation of nSMase2.bioRxiv : the preprint server for biology · 2025Article
- Chronic stress contributes to long-term isoflurane anesthesia-induced cognitive dysfunction via histone acetylation modulated by RbAp48-HDAC2 in male mice.Journal of anesthesia and translational medicine · 2025Article
- The multiple roles of chronic stress and glucocorticoids in Alzheimer's disease pathogenesis.Trends in neurosciences · 2024Review
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Chronic stress and elevated levels of glucocorticoids (GCs), the main stress hormones, accelerate Alzheimer's disease (AD) onset and progression. A major driver of AD progression is the spreading of pathogenic Tau protein between brain regions, precipitated by neuronal Tau secretion. While stress and high GC levels are known to induce intraneuronal Tau pathology (i.e. hyperphosphorylation, oligomerization) in animal models, their role in trans-neuronal Tau spreading is unexplored. Here, we find that GCs promote secretion of full-length, primarily vesicle-free, phosphorylated Tau from murine hippocampal neurons and ex vivo brain slices. This process requires neuronal activity and the kinase GSK3β. GCs also dramatically enhance trans-neuronal Tau spreading in vivo, and this effect is blocked by an inhibitor of Tau oligomerization and type 1 unconventional protein secretion. These findings uncover a potential mechanism by which stress/GCs stimulate Tau propagation in AD.
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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.