Boosting the expression of the ABCC1 gene may not only reduce amyloid plaques in the brain, it might also delay the onset of Alzheimer's disease. Read More
Microglia creates dense-core plaques which help to clear away more wispy plaques from neurons, preventing cell death. Findings suggest the dense-core plaques play a defensive role in protecting the brain from the ravages of neurodegenerative diseases, such as Alzheimer's. Read More
An increase in bad gum bacteria and a decrease in good bacteria is associated with amyloid-beta in cerebral spinal fluid samples of older adults. The findings add to the growing body of evidence linking periodontal disease to the development of Alzheimer's. Read More
Study reveals aluminum is co-located with the tau protein in people with familial Alzheimer's disease. Read More
The S198P mutation causes APP to fold more quickly, allowing amyloid-beta peptides to produce from mature APP at a more rapid rate than from APP that does not contain the genetic mutation. The findings shed new light on genetic mutations associated with Alzheimer's disease. Read More
Study reports tau accumulation in the temporal lobe was 75% higher in women than men. Read More
Exposing retinal pigment epithelium cells in mouse models to amyloid-beta resulted in retinal pathologies similar to those seen in human age-related macular degeneration. Read More
Regions of the olfactory system in mice with higher amyloid beta expression exhibited lower activation of olfactory sensory neurons and decreased odor detection. Read More
Over-expression of the synaptic protein RAPGEF2 drives synaptic loss associated with Alzheimer's disease. Read More
An antibody called HAE-4 targets APOE and removes Alzheimer's related amyloid plaques in mouse models. The antibody improves blood vessel function in the brain without raising the risk of brain bleeds. Read More
Amyloid-beta38 may have protective benefits against Alzheimer's disease, researchers report. Read More
Major surgery can trigger different patterns of cognitive alterations depending on previous presence, or absence, of Alzheimer's pathologies. Read More
