Detecting oligomers in the cerebrospinal fluid is no easy feat. The latest test is among the most sensitive yet, but is it useful?
Researchers have identified the striatum as a site of neurogenesis in the adult brain, but not in people with Huntington’s disease.
The FDA has stopped the personal genome sequencing company 23andMe from selling health assessments, saying its tests need validation. What do Alzheimer scientists think?
The antidepressant citalopram reduces agitation in Alzheimer’s patients, but caused abnormal heart rhythms at the tested dose.
A Phase 2 trial suggests that the drug PBT2 is generally safe for Huntington’s patients. The drug's sponsor says it may have improved cognition, though experts remain unconvinced.
Already linked to Alzheimer’s and other neurodegenerative diseases, a TREM2 variant now shows up on the ALS radar, too.
Mutant FUS meddles with RNA splicing and DNA damage repair in transgenic mice that succumb to disease.
It’s not just for tugging APP around the neuron: The SORLA receptor may also bind Aβ and hasten its demise.
Government, industry, and advocacy together will provide nearly $130 million for the identification of surrogate markers and targets.
In a cell culture system, astrocytes from people with ALS kill motor neurons. The model could yield more discoveries about the fundamental biology of this disease.
Live imaging of the mouse brain offers a rare view of α-synuclein dynamics at presynaptic terminals, and raises questions about which form of the protein triggers synaptic dysfunction.
A new grant opportunity will fund projects aimed at understanding the similarities and differences between biomarkers of Alzheimer’s and Parkinson’s diseases.
Aggressively treating high blood pressure and cholesterol in older adults with diabetes does not prevent cognitive decline, and results in more brain shrinkage.
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.
Proteins that interact with the Parkinson’s risk gene LRRK2 point to protein trafficking and degradation as causes of pathogenesis.