By targeting distinct cell populations in the external globus pallidus, researchers restore mobility to a mouse model of Parkinson’s disease.
Ionis announced top-line results of a Phase 3 trial of their drug for familial amyloid neuropathy. It met both primary endpoints but caused serious side effects in some people.
A new fluorescent compound labels only non-contractile cells in the capillary bed, supporting the idea that these mysterious little cells do not directly regulate brain blood flow.
Chronic, low-dose Δ9-tetrahydrocannabinal reset gene expression through epigenetics, increased the number of synapses, and reversed age-related memory loss. Young mice showed no benefit.
Examining multiple α-synuclein disorders in a Midwestern population shows that some kill faster than others. The worst: MSA.
On the contrary, having AD may lead to low body mass index, according to a genetic randomization study.
Researchers at AD/PD 2017 presented new data on an antibody and small molecules targeting amyloid.
Preparing the whole mouse head—not just the dissected brain—lets researchers analyze the neural tissue outside the skull that connects the nose to the inner sanctum.
A broadening drug development pipeline now contains Phase 1 or 2 drugs on targets unrelated to Aβ or tau.
The drug slows functional decline in patients with mild disease and should be available to U.S. patients in August.
A trial of an α-synuclein antibody is making use of the technology to follow subtle changes in the day-to-day function of participants.
Even without this important sidekick at hand, scientists are forging ahead with efficacy trials of their first attempts at disease-modification in Parkinson’s
Electrodes entering the brain through a hole above the jaw detected epileptic spikes in the hippocampi of Alzheimer’s patients. Scalp recordings missed the action.
Animal models suggest excessive NFκB-TNFα signaling brings on compulsive behavior in a frontotemporal dementia mouse model and early death in flies.
Found in familial and sporadic cases of ALS, mutations in the annexin A11 gene lead to elaborate protein clumps and seem to disrupt vesicular trafficking.