Smart Nanoparticles Reverse Alzheimer's Symptoms in Mice by Rebooting Brain Cleanup
Engineered nanoparticles cleared 50-60% of toxic amyloid plaques within 1 hour and restored the blood-brain barrier in Alzheimer's mice.
Aging biology, lifespan extension, hallmarks of aging, and healthspan optimization
2910 articles
Engineered nanoparticles cleared 50-60% of toxic amyloid plaques within 1 hour and restored the blood-brain barrier in Alzheimer's mice.
A completed Phase 2 trial investigates the immune mechanisms behind age-related vaccine failure in older adults.
Most genetic tests are probabilistic, not deterministic. Attia explains when DNA data truly changes decisions and when it just adds noise.
A comprehensive review reveals how the enzyme CD38 drives cardiovascular and neurological disease through calcium, NAD+, and inflammation signaling.
Chronic NAD depletion causes mitochondrial DNA to escape into the cytoplasm, activating an interferon response that mimics a viral infection.
A novel immune cell subset, CD38-high monocytes, spikes within 24 hours of sepsis onset and may serve as both a diagnostic marker and drug target.
A specialized immune cell population near adipose nerves declines with age, fueling inflammaging and disrupting fat metabolism.
Cholecystokinin prevents microglia from pruning excitatory synapses in sepsis brain injury, pointing to new cognitive protection strategies.
Nephropathic Cystinosis alters serum N-glycosylation patterns, especially sialylation, offering potential new disease biomarkers.
The FAIR-HF2 trial tested intravenous ferric carboxymaltose in iron-deficient heart failure patients, with surprising results for hard clinical endpoints.
A comprehensive 2025 review reveals how AMPK orchestrates mitochondrial fission, mitophagy, and biogenesis to restore cellular energy homeostasis.
GLP-1 receptor agonists like semaglutide activate AMPK signaling to reduce amyloid plaques and restore memory in Alzheimer's mouse models.