Stress as Both Risk and Mechanism in Alzheimer’s Disease: The Unruly Biomarker
How do chronic stress and breakdowns in stress neuroendocrine systems muddy the waters of Alzheimer’s disease causation, progression, and biomarker interpretation?
AI, biomarkers, and older-adult care. My notes on medical AI, dementia biomarkers, frailty, and older-adult care. This section is supported by my custom AI-assisted literature surveillance workflow that helps me identify recent papers that I then review. Each item is manually curated, edited, and approved before publication. The aim is not to summarize everything. The aim is to notice what may matter clinically, what is fragile, and what still needs to prove itself in real older-adult care.
How do chronic stress and breakdowns in stress neuroendocrine systems muddy the waters of Alzheimer’s disease causation, progression, and biomarker interpretation?
Does the rapid adoption of LLM-based AI tools by hospitalists translate into improved care, or does implementation quality still limit their clinical impact?
Can adaptive AI replicate human adjudication of cardiovascular events with adequate rigor to reduce trial workload without sacrificing accuracy?
Can a machine learning model built on routine blood counts and age reliably rule in or out clinically significant bone marrow fibrosis, reducing the need for invasive biopsy?
Is STAT3 a credible and actionable therapeutic target in Alzheimer’s disease, or just a marker of chronic neuroinflammation?
How do LLM-generated patient education materials for surgery care stack up on readability and real-world usability, especially for low-literacy patients?
Does a unified multi-modal model finally make AI image interpretation more grounded and interpretable for clinicians?
How does deep learning stack up against neurologist consensus for diagnosing acute lacunar stroke on CT perfusion—a notoriously difficult task, especially relevant for older adults?
How should health systems integrate amyloid PET into Alzheimer’s care after the rise of anti-amyloid therapies, and does the growing reliance on scanning clarify, or complicate, diagnosis and follow-up?
Can slow waves detected on resting EEG—outside of sleep—serve as accessible, early markers of amyloid pathology and neurodegeneration risk in Alzheimer’s disease?