1. Tissue model of Alzheimer's mimics beta-amyloid's effects on blood-brain barrier  News-Medical.net
  2. Blood pressure medication protects the BRAIN, too: Patients on high doses have 37% less damage  Daily Mail
  3. View full coverage on Google News
Beta-amyloid plaques, the protein aggregates that form in the brains of Alzheimer's patients, disrupt many brain functions and can kill neurons. They can also damage the blood-brain barrier — the normally tight border that prevents harmful molecules in the bloodstream from entering the brain.Beta-amyloid plaques, the protein aggregates that form in the brains of Alzheimer's patients, disrupt many brain functions and can kill neurons. They can also damage the blood-brain barrier — the normally tight border that prevents harmful molecules in the bloodstream from entering the brain.

Tissue model of Alzheimer's mimics beta-amyloid's effects on blood-brain barrier

Taking higher doses of blood pressure medication may slow down the development of white matter lesions - areas of age-related brain damage - linked to Alzheimer's, a new NIH study suggests.Taking higher doses of blood pressure medication may slow down the development of white matter lesions - areas of age-related brain damage - linked to Alzheimer's, a new NIH study suggests.

Blood pressure medication protects the BRAIN, too: Patients on high doses have 37% less damage | Daily Mail Online

The accumulation of aggregated amyloid-β (Aβ) in the brain is the first critical step in the pathogenesis of Alzheimer’s disease (AD), which also includes synaptic impairment, neuroinflammation, neuronal loss, and eventual cognitive defects. Emerging evidence suggests that impairment of Aβ phagocytosis and clearance is a common phenotype in late-onset AD. Rutin (quercetin-3-rutinoside) has long been investigated as a natural flavonoid with different biological functions in some pathological circumstances. Sodium rutin (NaR), could promote Aβ clearance by increasing microglial by increasing the expression levels of phagocytosis-related receptors in microglia. Moreover, NaR promotes a metabolic switch from anaerobic glycolysis to mitochondrial OXPHOS (oxidative phosphorylation), which could provide microglia with sufficient energy (ATP) for Aβ clearance. Thus, NaR administration could attenuate neuroinflammation and enhance mitochondrial OXPHOS and microglia-mediated Aβ clearance, ameliorating synaptic plasticity impairment and eventually reversing spatial learning and memory deficits. Our findings suggest that NaR is a potential therapeutic agent for AD.

Sodium rutin ameliorates Alzheimer’s disease–like pathology by enhancing microglial amyloid-β clearance | Science Advances