ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Posttraumatic stress disorder-like induction elevates β-amyloid levels, which directly activates corticotropin-releasing factor neurons to exacerbate stress responses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Traumatic Brain Injury and Alzheimer's Disease Biomarkers: A Systematic Review of Findings from Amyloid and Tau Positron Emission Tomography.Journal of neurotrauma · 2025Pooled it
- Evaluating the impact of intracerebroventricular norepinephrine on spatial memory in rats: Insights into sporadic Alzheimer's pathogenesis.IBRO neuroscience reports · 2026Article
- Neuropeptides in the Management of Alzheimer's Disease: From Pathophysiology to Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Sex differences in neuromodulatory subcortical systems and their implications for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Altered Functional Connectivity and Amyloid Deposition in Posttraumatic Stress Disorder-Associated Cognitive Impairment.AJNR. American journal of neuroradiology · 2025Article
- Hippocampal CA1 neuron, a crucial regulator for chronic stress exacerbating Alzheimer's disease progression.Cell & bioscience · 2025Article
- Multi-omics delineate growth factor network underlying exercise effects in an Alzheimer's mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Neurological, psychological, psychosocial complications of long-COVID and their management.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Association Between Body Mass Index and Comorbid Anxiety in First-Episode and Drug Naïve Patients With Major Depressive Disorder.Depression and anxiety · 2025Article
- Identification of novel risk genes for Alzheimer's disease by integrating genetics from hippocampus.Scientific reports · 2024Article
- Cognitive Effects of Simulated Galactic Cosmic Radiation Are Mediated by ApoE Status, Sex, and Environment in APP Knock-In Mice.International journal of molecular sciences · 2024Article
- Multi-omics delineate growth factor network underlying exercise effects in an Alzheimer's mouse model.bioRxiv : the preprint server for biology · 2024Article
- Potential Therapeutic Effects ofNutrients · 2024Article
- The Role of Insulin-like Growth Factor I in Mechanisms of Resilience and Vulnerability to Sporadic Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Life Experience Matters: Enrichment and Stress Can Influence the Likelihood of Developing Alzheimer's Disease via Gut Microbiome.Biomedicines · 2023Review
- Amyloid β-based therapy for Alzheimer's disease: challenges, successes and future.Signal transduction and targeted therapy · 2023Review
- Posttraumatic stress symptom severity predicts cognitive decline beyond the effect of Alzheimer's disease biomarkers in Veterans.Translational psychiatry · 2023Article
- Posttraumatic Stress and Traumatic Brain Injury: Cognition, Behavior, and Neuroimaging Markers in Vietnam Veterans.Journal of Alzheimer's disease : JAD · 2023Article
- Emerging Alzheimer's disease therapeutics: promising insights from lipid metabolism and microglia-focused interventions.Frontiers in aging neuroscience · 2023Review
- Influence of Cortisol on the Fibril Formation Kinetics of Aβ42 Peptide: A Multi-Technical Approach.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Recent studies have found that those who suffer from posttraumatic stress disorder (PTSD) are more likely to experience dementia as they age, most often Alzheimer's disease (AD). These findings suggest that the symptoms of PTSD might have an exacerbating effect on AD progression. AD and PTSD might also share common susceptibility factors such that those who experience trauma-induced disease were already more likely to succumb to dementia with age. Here, we explored these two hypotheses using a mouse model of PTSD in wild-type and AD model animals. We found that expression of human familial AD mutations in amyloid precursor protein and presenilin 1 leads to sensitivity to trauma-induced PTSD-like changes in behavioral and endocrine stress responses. PTSD-like induction, in turn, chronically elevates levels of CSF β-amyloid (Aβ), exacerbating ongoing AD pathogenesis. We show that PTSD-like induction and Aβ elevation are dependent on corticotropin-releasing factor (CRF) receptor 1 signaling and an intact hypothalamic-pituitary-adrenal axis. Furthermore, we show that Aβ species can hyperexcite CRF neurons, providing a mechanism by which Aβ influences stress-related symptoms and PTSD-like phenotypes. Consistent with Aβ causing excitability of the stress circuitry, we attenuate PTSD-like phenotypes in vivo by lowering Aβ levels during PTSD-like trauma exposure. Together, these data demonstrate that exposure to PTSD-like trauma can drive AD pathogenesis, which directly perturbs CRF signaling, thereby enhancing chronic PTSD symptoms while increasing risk for AD-related dementia.
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Registered trials
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.