Cancer Treatment Takes Aim at Tauopathy
Building on results in AD mouse models, researchers now report that immune checkpoint inhibitors reduce pathology and improve cognition in tauopathy mice, too. Other scientists are skeptical.
5724 RESULTS
Sort By:
Building on results in AD mouse models, researchers now report that immune checkpoint inhibitors reduce pathology and improve cognition in tauopathy mice, too. Other scientists are skeptical.
A failure to dispose of underperforming mitochondria may underlie the complex degenerative disorder known as multisystem proteinopathy...
Comprising mostly Aβ40, these large plaques are shot through with strange tubular structures and BBB markers. They are common in early onset AD.
In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
At AAT-ADPD, researchers report how they built on prior reports that a person’s blood level of p-tau181 tells if they have Alzheimer’s.
In 2,144 Colombian ADAD family members, plasma NfL in gene carriers rises as early as two decades before their symptoms start.
The method purportedly distinguishes patients from controls with more than 90 percent sensitivity and specificity.
The FDA has prioritized review of C2N’s blood test for amyloid-β. A pivotal clinical trial will correlate the test with amyloid PET scans.
With plasma tests performing in AIBL staging, scientists are sharing data across platforms and cohorts, and tackling standardization to avoid time lost to irreproducibility.
A Japanese company enters the arena with a plasma Aβ test that rivals CSF for detecting brain amyloid.
At SfN 2017, some of the lesser-known tau toxicities came in for deep scrutiny.
A simple blood draw may help distinguish garden-variety PD from other, less common parkinsonian disorders early in disease.
Despite no warning signs in ongoing clinical trials, researchers are searching for safer drugs, and better biomarkers to measure what they do.
Three studies agree that TMEM106b/progranulin double knockouts develop more extreme lysosomal dysfunction, inflammation, and motor deficits than PGRN KOs.
Viral surfaces attract proteins from the extracellular environment of the person they infect. This corona of host proteins makes the virus more or less infective—and promotes amyloid fibrils.