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.
Boosting sTREM2 in the brain rallied microglia to clear Aβ plaques, restored synaptic plasticity, and even rescued memory deficits in mice.
A newly uncovered population of astrocytes in layer V of the cortex modulate synapses by secreting a protein linked to Norrie disease, a form of blindness. Are other disease-related astroglia lurking in the brain?
Blocking the receptor clears toxic proteins and improves memory in old mice. The work proposes a new role in microglia for a well-known B-cell receptor.
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.
A prospective progeria drug revs up cellular autophagy and clears tau in neurons derived from patients with frontotemporal dementia. In mouse models, the drug rescues abnormal behavior.
Women who started menstruation after the age of 16, and/or entered menopause before 47, had higher rates of dementia later in life.