3,6’-dithiopomalidomide (DP), an anti-inflammatory drug candidate, protected mouse models of Alzheimer's disease against cognitive decline by reducing neuroinflammation.
Even for older people experiencing no general memory or thinking problems, performing poorly on a simple memory test may be linked to biomarkers for Alzheimer's disease.
Heart disease that causes brain dysfunction can lead to the development of Alzheimer's disease and triples the amount of amyloid-beta in the brain.
Microglia, a key immune cell in the brain, appears to mediate the relationship between the gut microbiome and amyloid-beta deposits in male mouse models of Alzheimer's disease.
A new framework reveals Alzheimer's disease is far more complex than previously believed. Rather than being a disease where the same causes produce the same outcomes, researchers found three different models for the disease, each with its own characterizations and dynamics.
Amyloid-beta accumulation in the brain may contribute to deficits in circadian regulation of learning and memory during the early stages of Alzheimer's disease.
Restoring normal sleep patterns by activating the thalamic reticular nucleus with chemogenetics reduced the accumulation of amyloid-beta plaques in the brains.
Older adults who sleep less than 4.5 hours, or more than 6.5 hours per night and who experience sleep disruptions are at greater risk of cognitive decline, researchers report.