ArticleLife science alliance2022
β-arrestin1 promotes tauopathy by transducing GPCR signaling, disrupting microtubules and autophagy.
Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Beta 2-adrenergic pathway combats Alzheimer's disease: Restoring cognition and synaptic integrity.Neural regeneration research · 2026Article
- Exercise Training Regulates Cortical GPCR-Mediated Signaling Networks Through cAMP, Calcium, and Neuroactive Ligand-Receptor Interaction Pathways in Diabetic-Obese Rats: An In Silico Study.International journal of molecular sciences · 2026Article
- Subtype-dependent arrestin engagement of the metabotropic glutamate receptors.Nature communications · 2026Article
- The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026Review
- The clinical implication of β-arrestins-mediated signaling in memory and cognition.Molecular and cellular biochemistry · 2025Review
- Implication of Central βArchiv der Pharmazie · 2025Review
- Proximity labeling reveals dynamic changes in the SQSTM1 protein network.bioRxiv : the preprint server for biology · 2024Article
- The influence of APOEActa neuropathologica · 2024Article
- Review
- Sex-dependent effects of acute stress on amyloid-β in male and female mice.Brain : a journal of neurology · 2023Article
- Interactions between β-arrestin proteins and the cytoskeletal system, and their relevance to neurodegenerative disorders.Frontiers in endocrinology · 2023Review
- Pathological characterization of a novel mouse model expressing the PD-linked CHCHD2-T61I mutation.Human molecular genetics · 2022Article
- Gq Signaling in Autophagy Control: Between Chemical and Mechanical Cues.Antioxidants (Basel, Switzerland) · 2022Review
- Biased β-Agonists Favoring Gs over β-Arrestin for Individualized Treatment of Obstructive Lung Disease.Journal of personalized medicine · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
G protein-coupled receptors (GPCRs) have been shown to play integral roles in Alzheimer's disease pathogenesis. However, it is unclear how diverse GPCRs similarly affect Aβ and tau pathogenesis. GPCRs share a common mechanism of action via the β-arrestin scaffolding signaling complexes, which not only serve to desensitize GPCRs by internalization, but also mediate multiple downstream signaling events. As signaling via the GPCRs, β2-adrenergic receptor (β2AR), and metabotropic glutamate receptor 2 (mGluR2) promotes hyperphosphorylation of tau, we hypothesized that β-arrestin1 represents a point of convergence for such pathogenic activities. Here, we report that β-arrestins are not only essential for β2AR and mGluR2-mediated increase in pathogenic tau but also show that β-arrestin1 levels are increased in brains of Frontotemporal lobar degeneration (FTLD-tau) patients. Increased β-arrestin1 in turn drives the accumulation of pathogenic tau, whereas reduced
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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.