Proteins that interact with the Parkinson’s risk gene LRRK2 point to protein trafficking and degradation as causes of pathogenesis.
Once considered a nuclear homebody, TDP-43 ventures out to accompany mRNAs down axons to nerve terminals where the transcripts can be turned into protein.
Government, industry, and advocacy together will provide nearly $130 million for the identification of surrogate markers and targets.
It’s not just for tugging APP around the neuron: The SORLA receptor may also bind Aβ and hasten its demise.
Mutant FUS meddles with RNA splicing and DNA damage repair in transgenic mice that succumb to disease.
The antidepressant citalopram reduces agitation in Alzheimer’s patients, but caused abnormal heart rhythms at the tested dose.
Researchers have identified the striatum as a site of neurogenesis in the adult brain, but not in people with Huntington’s disease.
The amyloid imaging agent florbetapir predicts cognitive decline much like its forerunner, PiB.
Older adults with amyloid in their brains develop abnormal activity in the entorhinal cortex even while memory and hippocampal function remain unaffected.
Death receptor role in Alzheimer's disease looks less likely than was originally thought following a high-profile paper in 2009.
New research suggests that α-synuclein comes in multiple strains, one of which seeds aggregation of tau.
In neurodegenerative disease, tau is in the dendrites, and scientists are beginning to flesh out ways to block what it does there.
New research strengthens the idea that microglia do far more than scour the brain for emergencies.
Researchers have co-opted a molecular transport system to shuttle Aβ antibodies across the mouse blood-brain barrier. They predict the shuttle could smuggle a variety of drugs into the brain.
A small study suggests that exposure to the pesticide DDT heightens the risk of developing Alzheimer’s disease.