Using theranostics to pinpoint and treat the earliest, preclinical symptoms of Alzheimer's disease, researchers say their new method shows promise in stopping the progression of Alzheimer's pathologies before the onset of irreversible neural damage.
Researchers discovered a correlation between obesity-related neurodegeneration and Alzheimer's disease pathology. Losing weight, they say, can slow age-related cognitive decline and reduce the risk of developing Alzheimer's.
Study provides experimental evidence of an alternative binding site on amyloid-beta aggregates. The discovery opens the door to the development of new therapies for Alzheimer's disease.
Samples of brain tissue from those with Alzheimer's revealed marked changes in potassium isotopes that correlated with amyloid-beta accumulation.
The brains of older, cognitively healthy people have similar amounts of dissolvable, non-fibrilla amyloid proteins as the brains of those with Alzheimer's disease. Findings challenge the long-standing theory that having higher levels of amyloid proteins is an underlying cause of Alzheimer's disease.
Lecanemab, an amyloid-clearing monoclonal antibody drug shows positive results in the treatment of Alzheimer's disease. The drug is now poised for FDA approval early in 2023. Lecanemab slows cognitive decline by 27%.
A new study reveals it is not only possible to determine Alzheimer's risks before symptoms appear, but it is also possible to determine who will deteriorate within the next few years.
Deletion of the neurodegenerative disease associated microglial gene CX3CR1 aggravated the disease state and increased the accumulation of plaques in the brains of mouse models of Alzheimer's disease. Deficiencies of the gene also impaired the movement of microglia toward the plaques.
An intranasally delivered oxytocin derivative helped improve cognitive function and reduced cognitive impairment in mouse models of Alzheimer's disease.