ArticleMolecular neurobiology2016
Tau Mislocation in Glucocorticoid-Triggered Hippocampal Pathology.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Tracheal aspirates of mechanically ventilated preterm infants possess cytopathic tau variants: a prospective exploratory study.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- The multiple roles of chronic stress and glucocorticoids in Alzheimer's disease pathogenesis.Trends in neurosciences · 2024Review
- Glucocorticoid stress hormones stimulate vesicle-free Tau secretion and spreading in the brain.Cell death & disease · 2024Article
- Sex Differences in Stress Response: Classical Mechanisms and Beyond.Current neuropharmacology · 2024Article
- Chronic Stress, Depression, and Alzheimer's Disease: The Triangle of Oblivion.Advances in experimental medicine and biology · 2023Article
- Chronic pain causes Tau-mediated hippocampal pathology and memory deficits.Molecular psychiatry · 2022Article
- Therapeutic Targeting of Rab GTPases: Relevance for Alzheimer's Disease.Biomedicines · 2022Review
- Rab35 and glucocorticoids regulate APP and BACE1 trafficking to modulate Aβ production.Cell death & disease · 2021Article
- Allosteric modulation of AMPA receptors counteracts Tau-related excitotoxic synaptic signaling and memory deficits in stress- and Aβ-evoked hippocampal pathology.Molecular psychiatry · 2021Article
- Sex Hormone Depletion Augments Glucocorticoid Induction of Tau Hyperphosphorylation in Male Rat Brain.Neuroscience · 2021Article
- Where Dopaminergic and Cholinergic Systems Interact: A Gateway for Tuning Neurodegenerative Disorders.Frontiers in behavioral neuroscience · 2021Review
- Dendritic/Post-synaptic Tau and Early Pathology of Alzheimer's Disease.Frontiers in molecular neuroscience · 2021Review
- Article
- Dysregulation of autophagy and stress granule-related proteins in stress-driven Tau pathology.Cell death and differentiation · 2019Article
- Risk Factors for Alzheimer's Disease: Focus on Stress.Frontiers in pharmacology · 2019Review
- Activated PPARγ Abrogates Misprocessing of Amyloid Precursor Protein, Tau Missorting and Synaptotoxicity.Frontiers in cellular neuroscience · 2019Article
- Regulation of Tau Protein on the Antidepressant Effects of Ketamine in the Chronic Unpredictable Mild Stress Model.Frontiers in psychiatry · 2019Article
- Endolysosomal degradation of Tau and its role in glucocorticoid-driven hippocampal malfunction.The EMBO journal · 2018Article
- Atypical, non-standard functions of the microtubule associated Tau protein.Acta neuropathologica communications · 2017Review
- Altered metabotropic glutamate receptor 5 markers in PTSD: In vivo and postmortem evidence.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The exposure to high glucocorticoids (GC) triggers neuronal atrophy and cognitive deficits, but the exact cellular mechanisms underlying the GC-associated dendritic remodeling and spine loss are still poorly understood. Previous studies have implicated sustained GC elevations in neurodegenerative mechanisms through GC-evoked hyperphosphorylation of the cytoskeletal protein Tau while Tau mislocation has recently been proposed as relevant in Alzheimer's disease (AD) pathology. In light of the dual cytoplasmic and synaptic role of Tau, this study monitored the impact of prolonged GC treatment on Tau intracellular localization and its phosphorylation status in different cellular compartments. We demonstrate, both by biochemical and ultrastructural analysis, that GC administration led to cytosolic and dendritic Tau accumulation in rat hippocampus, and triggered Tau hyperphosphorylation in epitopes related to its malfunction (Ser396/404) and cytoskeletal pathology (e.g., Thr231 and Ser262). In addition, we show, for the first time, that chronic GC administration also increased Tau levels in synaptic compartment; however, at the synapse, there was an increase in phosphorylation of Ser396/404, but a decrease of Thr231. These GC-triggered Tau changes were paralleled by reduced levels of synaptic scaffolding proteins such as PSD-95 and Shank proteins as well as reduced dendritic branching and spine loss. These in vivo findings add to our limited knowledge about the underlying mechanisms of GC-evoked synaptic atrophy and neuronal disconnection implicating Tau missorting in mechanism(s) of synaptic damage, beyond AD pathology.
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Registered trials
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