ArticleNeurobiology of stress2020
Reproductive status impact on tau phosphorylation induced by chronic stress.
Article in Neurobiology of stress, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- 14-3-3γ Protects Against Postoperative Cognitive Dysfunction by Regulating Tau Thr205 Phosphorylation and Synaptic Integrity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuroprotective effect of selenium in rats subjected to chronic intermittent cold and immobilization stress: The role of phosphorylated tau.Iranian journal of basic medical sciences · 2026Article
- Research Progress on the Etiology and Pathogenesis of Alzheimer's Disease from the Perspective of Chronic Stress.Aging and disease · 2023Review
- Liuwei Dihuang formula ameliorates chronic stress-induced emotional and cognitive impairments in mice by elevating hippocampal O-GlcNAc modification.Frontiers in neuroscience · 2023Article
- Restraint Stress Delays the Recovery of Neurological Impairments and Exacerbates Brain Damages through Activating Endoplasmic Reticulum Stress-mediated Neurodegeneration/Autophagy/Apopotosis post Moderate Traumatic Brain Injury.Molecular neurobiology · 2022Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Sex and exposure to chronic stress have been identified as risk factors for developing Alzheimer's disease (AD). Although AD has been demonstrated to be more prevalent in females, sex is often overlooked in research studies, likely due to the complexity of the hormonal status. In female rats, the reproductive status can modulate the well-known increase in tau phosphorylation (pTau) caused by the exposure to acute physical and psychological stressors. To test the hypothesis that reproductive status can impact hippocampal pTau induced by chronic stress, cohorts of virgin, lactating (4-5 days pp), and post-maternal (1-month post-weaned) rats were subjected to a daily 30-min episode of restraint stress for 14 days and were sacrificed either 20 min or 24 h after their last stress/handling episode. Western blot analysis of two well-characterized AD-relevant pTau epitopes (AT8 and PHF-1) and upstream pTau mechanisms (e.g. GSK3β) analysis, showed that stressed post-maternal rats have increased pTau in comparison to stressed lactating rats 20 min after their last stress episode. Furthermore, an increase in pTau was also seen 24 h after the last stress episode in stressed post-maternal rats in comparison to their non-stressed controls in the detergent-soluble fraction. GSK3 analysis showed an increase in total levels of GSK3β in virgin rats and an increase of inactive levels of GSK3β in post-maternal rats, which suggests a different stress response in pTau after the rat has gone through the maternal experience. Interestingly, post-maternal rats also presented the more variability in their estrous cycles in response to stress. Besides no differences in pTau, non-stressed lactating rats showed an increase in inactive GSK3β 24 h after the last handling episode. Immunohistochemical detection of the PHF-1 epitope revealed increased pTau in the CA4/hilar subfield of the hippocampus of virgin and post-maternal rats exposed to chronic stress shortly after their last stress episode. Overall, lactating rats remained unresponsive to chronic restraint stress. These results suggest increased sensitivity of the virgin and post-maternal rats to hippocampal stress-induced pTau with chronic restraint stress compared to lactating rats. Because no differences were detected in response to stress by lactating rats and an exaggerated response was observed in post-maternal rats, current results support the hypothesis that lactation affects tau processing in the brain of the female.
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