A deletion in chromosome 22 points to new genetic risk factors for Parkinson's disease.
Amyloid fibrils seeded by Alzheimer’s brain extracts indicate that Aβ forms specific strains in different individuals.
A new study supports the idea that non-motor symptoms of Parkinson's disease may aid earlier diagnosis.
New imaging data suggests degeneration of the fornix could help identify seniors on the verge of cognitive decline.
Older people improved memory and attention after playing a challenging video game, supporting the idea that multitasking could have benefits for cognition.
New research connects extracellular Aβ to intracellular kinases that mediate its toxicity.
The insoluble proteome from Alzheimer’s brains points to RNA processing proteins as a novel component of aggregates.
As heat shock protein and co-chaperone team up to shield tau from degradation, they create toxic oligomers.
Fueling (or rekindling) controversy over anti-aging benefits of sirtuins, researchers report that Sirt1 lengthens lifespan in mice.
Without the protein beclin 1, rapacious microglia choke on amyloid β.
Researchers nabbed rare variants in Alzheimer’s genes by sequencing DNA from people with very high or very low levels of cerebrospinal fluid biomarkers.
Preliminary data from Parkinson’s Progression Markers Initiative suggests that cerebrospinal fluid biomarkers distinguish the most rapidly progressing form of Parkinson’s.
In sporadic and familial Parkinson's, faulty parkin may damage dopamine neurons by letting a deadly protein linger.
Researchers say that analyzing long stretches of homozygosity in people of Caribbean Hispanic descent represents an approach to finding rare, recessive Alzheimer’s mutations.
Functional genomics and mouse analyses blame waning levels of histone-binding protein for memory loss in aging.