ReviewFrontiers in pharmacology2019
Risk Factors for Alzheimer's Disease: Focus on Stress.
Review in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Evaluating the impact of intracerebroventricular norepinephrine on spatial memory in rats: Insights into sporadic Alzheimer's pathogenesis.IBRO neuroscience reports · 2026Article
- APOE4 exacerbates glucocorticoid stress hormone-induced tau pathology via mitochondrial dysfunction.Cell death & disease · 2026Article
- Sex differences in neuromodulatory subcortical systems and their implications for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Investigating shared risk variants and genetic etiology between Alzheimer's disease and three stress-related psychiatric disorders: a large-scale genome-wide cross-trait analysis.Frontiers in aging · 2025Article
- Ultrastructural features of psychological stress resilience in the brain: a microglial perspective.Open biology · 2024Review
- Sex-specific associations of serum cortisol with brain biomarkers of Alzheimer's risk.Scientific reports · 2024Article
- 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
- Intracerebral inoculation of healthy non-transgenic rats with a single aliquot of oligomeric amyloid-β (1-42) profoundly and progressively alters brain function throughout life.Frontiers in aging neuroscience · 2024Article
- Alzheimer's Disease: Significant Benefit from the Yeast-Based Models.International journal of molecular sciences · 2023Review
- Altered Mitochondrial Morphology and Bioenergetics in a New Yeast Model Expressing Aβ42.International journal of molecular sciences · 2023Article
- The complex relationship between obesity and neurodegenerative diseases: an updated review.Frontiers in cellular neuroscience · 2023Review
- Involvement of brain-derived neurotrophic factor signaling in the pathogenesis of stress-related brain diseases.Frontiers in molecular neuroscience · 2023Review
- Altered Blood and Brain Expression of Inflammation and Redox Genes in Alzheimer's Disease, Common to APPInternational journal of molecular sciences · 2022Article
- Alzheimer's Disease and Specialized Pro-Resolving Lipid Mediators: Do MaR1, RvD1, and NPD1 Show Promise for Prevention and Treatment?International journal of molecular sciences · 2020Review
- A Comprehensive, Multi-Modal Strategy to Mitigate Alzheimer's Disease Risk Factors Improves Aspects of Metabolism and Offsets Cognitive Decline in Individuals with Cognitive Impairment.Journal of Alzheimer's disease reports · 2020Article
- Contributions of DNA Damage to Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Cholinergic Modulation of Glial Function During Aging and Chronic Neuroinflammation.Frontiers in cellular neuroscience · 2020Review
- Interaction of Tau with the chemokine receptor, CX3CR1 and its effect on microglial activation, migration and proliferation.Cell & bioscience · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In vulnerable individuals, chronic and persistent stress is an established risk factor for disorders that are comorbid with Alzheimer's disease (AD), such as hypertension, obesity and metabolic syndrome, and psychiatric disorders. There are no disease-modifying drugs in the treatment of AD, and all phase-3 clinical trials with anti-amyloid drugs (e.g., β- or γ-secretase inhibitors and monoclonal antibodies) did not meet the primary endpoints. There are many reasons for the lack of efficacy of anti-amyloid drugs in AD, the most likely being a late start of treatment, considering that pathophysiological mechanisms underlying synaptic dysfunction and neuronal death begin several decades before the clinical onset of AD. The identification of risk factors is, therefore, an essential step for early treatment of AD with candidate disease-modifying drugs. Preclinical studies suggest that stress, and the resulting activation of the hypothalamic-pituitary-adrenal axis, can induce biochemical abnormalities reminiscent to those found in autoptic brain samples from individuals affected by AD (e.g., increases amyloid precursor protein and tau hyperphosphorylation). In this review, we will critically analyze the current knowledge supporting stress as a potential risk factor for AD.
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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.