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.
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.
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.
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?
Speakers at AD/PD 2019 reported that AD risk factors mess up lipid metabolism in glial cells. In cellular models, speeding the clearance of fats lessened pathology.
People who take leisurely walks, garden, and tackle household chores had bigger brains than those who were more sedentary. Vigorous exercise brought neither additional benefit nor harm.
Scientists know that the retina changes in people with preclinical AD; alas, there is neither consensus nor convergence in the field of retinal imaging. An upcoming initiative aims to determine which measures are most robust.