A bit less strapped for funding, researchers are considering the next steps for Lewy body, frontotemporal, and vascular dementia.
NAPA's latest collective exercise was a conference to update the field on progress in the past three years and advise the NIH on how to spend the next round of funds.
At Athens meeting, scientists had new data on where these species appear in the brain, how they disrupt neurons, and whether oligo-specific antibodies would work.
Results raise the tentative prospect that a medical food might have possible cognitive benefit early in disease.
AV1451 appears too weak to diagnose non-AD tauopathies.
Preliminary data suggests a long lag between Aβ and tau deposits as the disease develops.
Using PET, researchers are trying to match tau spread against structural and functional defects.
The prion concept continues to infiltrate the neurodegeneration field, with models of SOD1 propagation and a bevy of tau strains.
The drug benefits some patients with mild amyotrophic lateral sclerosis, and is approved in Japan.
When clinicians and pathologists argue, sometimes genetics can settle the dispute. How about DLB?
How α-synuclein aggregates spread, quite possibly starting in the nose in some people, sets DLB apart from its better-known cousins, Alzheimer’s and Parkinson’s.
In dementia with Lewy bodies, basic scans are used in routine diagnosis. Multimodal imaging and new PET tracers for affected neurotransmitters of pathological deposits in the brain and gut are entering research settings.
At a DLB meeting, scientists reported progress in disentangling the notorious overlap in symptoms and pathology in this quintessential spectrum disease. (Hint: tangles are bad.)
Studies find that a drug in cough syrup can improve symptoms, and that radiation therapy safely shuts off a salivary gland.
At the International Dementia with Lewy Bodies conference in Fort Lauderdale, Florida, fuzzy images of dying sympathetic cardiac nerve terminals proved to be a sharp aide to clinch this notoriously difficult diagnosis.