CRISPR Suppresses BACE1 and Plaques in Mice
Deleting BACE1 with CRISPR nanocomplexes tempered Aβ pathology and boosted memory.
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Deleting BACE1 with CRISPR nanocomplexes tempered Aβ pathology and boosted memory.
With three trials and initiatives to boost recruitment, GAP-Net is gaining some traction in the field.
In Year Three, GAP Trial Network Is Starting to Hum Getting to Go: GAP-Net Sets Sight on Faster Start Three years after the Global Alzheimer’s Platform (GAP) Foundation launched GAP-Net, a standing network of clinical trial sites optimized for Alzheimer’s
From central IRBs, certified raters, to local transport: Changes large and small are needed to ramp up drug testing in Alzheimer’s.
Among 20 focus areas, 47 research recommendations cover the gamut from basic science to health disparities.
Award recognizes his contributions to basic and clinical research.
Experts said Phase 3 data did not prove the device could slow AD.
A majority of amyloid PET scans led physicians to change how they managed a patient’s disease. The effect on later outcomes is yet to be come.
Transcranial, alternating electrical current restored neuronal synchrony in older people, rejuvenating working memory. For an hour or two.
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.
Institute to chart new translational research territory.
After years of grunt work on next-gen sequencing and expression analysis, geneticists are finally reaping results. The new genes underscore the role of known pathways and cell types in disease.
At AD/PD Conference, New Alzheimer’s Genes Reinforce Known Pathways Expression, Expression, Expression—Time to Get on Board with eQTLs APP Upp: Mutation Nixes Six Amino Acids from Aβ, Spurs Aggregation Parsing How Alzheimer’s Genetic Risk Works Through Mi
A tool of modern genetics, expression studies link GWAS hits to specific cell types, providing clues to pathogenesis. Microglia come up again and again.
Presented at AD/PD, the discovery by scientists in Uppsala is the first APP deletion found to cause Alzheimer’s disease. The same group found the Swedish and Arctic APP mutations.
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