The acetylcholinesterase inhibitor failed to slow cognitive decline in people with both depression and mild cognitive impairment.
Data from the first human study hints the procedure could help deliver drugs to the brain, or even work as a therapy in its own right. A flurry of animal studies presented at AAIC support the idea.
In mice, aggregates of oxidized SOD1 accumulated with age, and endoplasmic reticulum stress made it worse. Does this explain SOD1 aggregates found in spinal cords of patients with sporadic ALS?
The hippocampus trickles out new neurons throughout life, a process that falters without BACE1 or in the presence of ApoE4.
In SPRINT MIND trial, strict control of systolic pressure slashed MCI incidence by almost 20 percent.
UCB-J hints at early synaptic loss in the hippocampus, but not the cortex. Researchers puzzle over the pattern.
Analyzing Phase 2 trial CSF of an investigational immunotherapy, scientists showed for the first time that treatment mitigates neurotoxic oligomers in patients.
Aging lymphatic vessels in the meninges hinder waste clearance from the brain and exacerbate Aβ build-up.
The findings offer one way this RNA-binding protein gets into cytoplasm, where it sets the stage for pathological aggregation.
BAN2401 Removes Brain Amyloid, Possibly Slows Cognitive Decline On Target: Crenezumab Reduces Aβ Oligomers in CSF PET Ligand Lights Up AAIC, May Detect Synapse Loss in AD Could Better Blood Pressure Management Preserve Cognition? Focused Ultrasound ...
Researchers consider the data encouraging, though questions linger about the cognition results. Did regulators mess up the randomization of this trial?
By loosening their chromatin straitjackets, and reining in their RNA watchdogs, tau unleashes transposable elements into the genome.
Investors pledge new money for research into biomarkers that yield marketable tests.
Oligonucleotides that suppress SOD1, and small molecules that limit its binding to the protein Derlin-1, delay disease onset and extend lifespan in rodent models of ALS.
In knockouts that model the most severe form of Gaucher’s disease, replacing one gene calms neuroinflammation, reduces neurodegeneration, and extends lifespan.