New data suggest that while peptides translated from an expansion in the C9ORF72 gene are toxic, they don’t directly interfere with nucleocytoplasmic transport.
No link found with amyloid deposition.
The same endothelial cell response is found in various models of brain disease.
Brain biopsy tissue reveals that their transcriptomes shift by location, age, and disease.
In a mouse tauopathy model, knocking out the NLRP3 inflammasome prevented toxic tau from forming.
Based on preclinical data, researchers gave this antibiotic a shot in a two-year clinical trial. It did nothing to slow cognitive decline.
Encouraged by success in treating infant spinomuscular atrophy, researchers are redoubling their efforts to target genetic causes of age-related neurodegeneration.
While former professional soccer players have less risk for heart disease and cancer than the general population, they are five times more likely to die with a neurodegenerative disease in old age.
In PASSPORT study, the antibody failed to slow progressive supranuclear palsy. Alzheimer’s trial to continue.
Prior research has focused on microglia interacting with synapses. New data show they also deal directly with the neuronal cell body. Like little conference rooms, specialized junctions host this communication.
As gene therapy is making a comeback, scientists are exploring if it might prevent or reverse Alzheimer’s. Some of those treatments are permanent, heightening safety concerns.
Using mass spectrometry to detect teensy amounts of phospho-tau species in plasma, researchers reported that p-tau-217 and p-tau-181 picked out people with Aβ pathology. Differences between groups appear to be huge. An MS-based test for plasma Aβ42 corresponded to brain amyloid, and is going in for regulatory approval.
Researchers link age-related weakening of the barrier to TGFβ signaling, hyperexcitation, and cognitive problems. In rodents, TGFβ antagonists attenuate these effects, reducing seizures.
Apabetalone, an epigenetic drug that tamps down vascular inflammation, slowed cognitive decline in people with MCI. A new statistical analysis of results from AMBAR claimed the plasma-exchange therapy might boost cognition by removing pathogenic proteins from blood.
While gene-based therapy for late-onset AD may seem distant, rare neurological disorders could point the way.