Study finds amyloid-beta plaques may not be the cause of memory loss associated with Alzheimer's disease, but instead a consequence of the disease. Regardless of the levels of amyloid plaques, researchers found individuals with high levels of amyloid peptide were cognitively normal. Higher levels of soluble amyloid beta peptide were also linked to people having a larger hippocampus.
P-glycoprotein, a critical toxin pump in the body, has the ability to remove amyloid plaques from the brain. Researchers say increasing P-gp in the blood-brain barrier of those at risk for Alzheimer's could postpone or prevent the onset of the neurodegenerative disease.
Study reveals the significant role lipids play in regulating the amyloid pathway protein C99 and the progression of Alzheimer's disease.
The connection between brain activity during sleep and cerebrospinal fluid flow was reduced in those with risk factors for dementia and those with Alzheimer's disease than in the healthy control group.
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.
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.
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.
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.
Study reports tau accumulation in the temporal lobe was 75% higher in women than men.