ArticleNature communications2025
Chromogranin A deficiency attenuates tauopathy by altering epinephrine-alpha-adrenergic receptor signaling in PS19 mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed.
- A non-canonical androgen signaling pathway drives microglial activation and tau pathology in females.Research square · 2026Article
- Catestatin peptide impedes melanoma progression and drug resistance by reprogramming oncogenic signaling pathways.Oncogenesis · 2026Article
- AI guided discovery of a murine model of asymptomatic Alzheimer's disease.Acta neuropathologica communications · 2026Article
- Ketone body β-hydroxybutyrate restores neuronal Tau proteostasis via ketolysis-independent mechanism.bioRxiv : the preprint server for biology · 2026Article
- Catestatin peptide impedes melanoma progression and drug resistance by reprogramming oncogenic signaling pathways.Research square · 2026Article
- Chromogranin A and catestatin regulate pancreatic islet homeostasis, endocrine function, and neurotransmitter signaling.Communications biology · 2025Article
- Comparative Investigation of the Retinal Phenotype of Three Mouse Models of Alzheimer's Disease With Optical Coherence Tomography.Investigative ophthalmology & visual science · 2025Article
- Catestatin suppresses melanoma progression and drug resistance through multitargeted modulation of signaling pathways.bioRxiv : the preprint server for biology · 2025Article
- Boolean Network Modeling Identifies Cognitive Resilience in the First Murine Model of Asymptomatic Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- Regulation of granin neuropeptide gene expression in human brain during development.Frontiers in molecular neuroscience · 2025Article
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Abstract
Metabolic disorders such as insulin resistance and hypertension are potential risk factors for aging and neurodegenerative diseases. These conditions are reversed in Chromogranin A (CgA) knockout (CgA-KO) mice. CgA is known to be associated with protein aggregates in the brains of neurodegenerative diseases including Alzheimer's disease (AD). Here, we investigated the role of CgA in Tau pathogenesis in AD and corticobasal degeneration (CBD). CgA ablation in Tauopathy mice (PS19) (CgA-KO/PS19) reduced pathological Tau aggregation and spreading, extended lifespan, and improved cognitive function. Transcriptomic and metabolite analysis of mouse cortices revealed elevated alpha-1-adrenergic receptors (Adra1) expression and high Epinephrine (EPI) levels in PS19 mice compared to WT mice, mirroring observations in AD and CBD patients. CgA depletion in PS19 mice lowered cortical EPI levels and the expression of Adra1 back to normal. Treatment of WT hippocampal organotypic slice cultures with EPI or Adra1 agonist promoted, while an Adra1 antagonist inhibited Tau hyperphosphorylation and formation of neurofibrillary tangles, which is unaltered upon CgA depletion. These findings demonstrate the involvement of CgA in Tau pathogenesis and highlight the interplay between the EPI-Adra1 signaling pathway and CgA in Tauopathy.
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