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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 ...
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.
In Taiwan, interferon treatment for chronic hepatitis C infection appears to have reduced the incidence of Parkinson’s disease.
Expression of VCAM1 on the endothelial cells that line the blood-brain barrier allowed aging factors in the plasma to exact their toll on the brain.
By slipping human microglia inside the mouse brain, researchers hope to better monitor their response to pathologies, such as Aβ.
Researchers publish 14 new AD variants. This includes one near WWOX, a gene that encodes a protein linked to tau and lipid metabolism.
Human cells show more phenotypic variation than mouse microglia, but the two match up well overall.
Longitudinal and genetic studies reveal that intelligence underlies cognitive reserve.
Many genes that increase risk for late-onset AD are expressed in microglia, and researchers are going cell by cell to unravel the pathways involved in the immune response to amyloid and tau.
At SfN and in new papers, scientists describe how synapses crater under the combined onslaught of Aβ and tau. They also link gene-expression signatures to the selective vulnerability of excitatory neurons to tau pathology.
Aggregates that form inside, or just pass through, oligodendrocytes take on the properties of the virulent strain that gives rise to multiple system atrophy.
