Inhibiting the receptor activates microglia to mop up debris, making CD33 an attractive therapeutic target.
Scientists at AD/PD 2019 see a Goldilocks of microglial activation: Both too little and too much is bad in an injured brain. How could a therapy make it just right?
In people carrying two mutated copies of the trophic receptor, important brain structures, such as the corpus callosum, never developed.
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.
The method purportedly distinguishes patients from controls with more than 90 percent sensitivity and specificity.
A tool of modern genetics, expression studies link GWAS hits to specific cell types, providing clues to pathogenesis. Microglia come up again and again.
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 ...
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.
Institute to chart new translational research territory.
Flortaucipir in former NFL players cropped up in regions known to be affected by chronic traumatic encephalopathy, but uptake was low compared with AD. Whether this reflects low tau deposition or poor tracer binding remain to be seen.
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.
The latest effort to determine if a non-steroidal anti-inflammatory drug protects against Alzheimer’s posted negative results. Time to abandon the approach?
The Phase 3 trial ended early when prodromal AD patients on the BACE1 inhibitor declined faster than those on placebo.
Senolytic drugs kill these cells, temper Aβ, and improve cognition in transgenic mice.
Transcranial, alternating electrical current restored neuronal synchrony in older people, rejuvenating working memory. For an hour or two.