Liquid droplets of tau subsume and concentrate tubulin, which then rapidly forms microtubules.
Dopaminergic neurons made from human iPS cells take root in monkey brains and reverse PD-like motor problems. Matching donor and host immune signatures mitigates graft rejection.
Agonists of β2-adrenergic receptor dampened transcription of α-synuclein, and protected neurons in mice and patient cells. Norwegians taking the drugs had half the risk of PD.
Large study using GAAIN data reveals subtle sex differences in chances for AD.
Somatic mutations in microglial progenitors trigger a neurodegenerative disease in mice. What about in people?
In a pilot study, a curcumin-based probe allowed researchers to detect retinal amyloid deposits in AD patients, but it remains to be seen if this can serve as an early biomarker.
Researchers identify where proteases snip the microglial receptor TREM2 to release its extracellular domain: exactly at the site of a rare AD risk variant.
About half of microglia in the mouse brain live as long as the whole mouse, while those in the human brain live, on average, just over four years. How does this change in Alzheimer’s?
Phase 1 clinical data presented at AAIC 2017 suggest few serious adverse events.
Three BACE inhibitors, a γ-secretase modulator, and a phosphodiesterase inhibitor appeared safe in Phase 1 trials.
Idalopirdine is out. Next up, a handful of secretase inhibitors, other small molecules, and immunotherapies for Aβ and tau seem safe in Phases 1 and 2.
Researchers at AAIC presented several imaging measures that may help explain the phenomenon of preserved cognition in the face of AD pathology.
Hsp90, a protein chaperone that helps misfold tau, enlists the co-chaperone Aha1 in the process. Could crippling Aha1 reduce tau aggregation?
Danish study correlates higher natural levels of lithium to lower incidence of Alzheimer’s disease
Tamping down a cell stress response saves neurons from degenerating while helping mice retain both their strength and their wits.