By aging cultured neurons and manipulating them to stimulate endocytosis or interfere with vesicle release, researchers can bring about characteristics of Alzheimer’s—without adding APP or Aβ.
Researchers no longer debate whether misfolded proteins spread through the brain in neurodegenerative disease. Now they want to know how.
Apolipoprotein E4 clearly plays a role in AD and could be a therapeutic target, but scientists are not sure whether they should raise or lower it in the brain...
At AD/PD 2019, scientists implicated both peripheral and central innate immunity in promoting propagation.
The global agency’s report recommends physical activity, a healthy diet, stopping alcohol abuse and smoking, and managing one’s weight, blood pressure, and diabetes.
Institute to chart new translational research territory.
In a new, inducible mouse model, poly(GR) damages mitochondria, but its effect is reversible. In flies, turning off transcription of hexanucleotide expansion protects cells.
Antisense Oligonucleotides: Can They Take on ALS, SMA, Prions? American Academy of Neurology 2019 Annual Meeting ...
As RNA Therapies Come of Age, Efficacy Remains Weak At AAN, Sights Set on Antisense Therapies for Diseases of the Brain New Alzheimer’s and Parkinson’s Immunotherapy Data at AAN Will RNA molecules that bump up or tamp down gene expression live up to their ...
Data on ASOs, presented recently at the annual meeting of the American Academy of Neurology, depict RNA-based therapies as broadly on the rise in neurodegenerative diseases.
A fleet of patient-derived neurons show that while an APP mutation shifts where γ-secretase takes its first bite, PS1 mutations blunt the enzyme’s second cut. Eventually, all mutations drive up the Aβ42:40 ratio.
Research on postmortem human brain strengthens the idea that an ebbing of neurogenesis may underlie cognitive decline.
Phase 1b data show that Biogen’s BIIB092 lowers N-terminal tau fragments in cerebrospinal fluid by more than 90 percent.
In a mouse model of frontotemporal dementia, a trifecta of tau mutations hobbles newborn neurons in the dentate gyrus.
A compound that only blocks presenilin 1-containing secretases beat back leukemia in mice—without side effects caused by broad-spectrum inhibitors.