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.
AAIC presentations identified early imaging changes in aging and AD, and reinforced the idea that CSF markers change little over the short term.
TIA1 mutations promote phase separation, generate a signature TDP-43 pathology.
Rather than changing one by one, many biomarkers—including cognition, tau PET, hippocampal atrophy, and CSF p-tau—shift together, around the time of symptom onset in young adults with familial AD.
Another paper reports that tau forms liquid droplets, and does so more readily when phosphorylated. What this portends for tangle formation inside of neurons remains to be seen.
Progranulin yields multiple granulins in cells that persist in lysosomes and could be key to preventing FTD.
Progenitors in cortical spheroids, cultured for nearly two years, morph into mature astrocytes, allowing researchers to study this process in vitro.
At AAIC 2017, scientists offered new clues on sleep and AD neuropathology. They identified parts of the brain that may be involved and highlighted the benefits of treating sleep disorders.
Motor symptoms slightly improved in 31 patients taking exenatide for 48 weeks, while the placebo group worsened. The effect persisted three months after treatment stopped.
Injecting a piece of this anti-aging protein days before memory testing improved performance in mice young and old, as well as those that overexpress α-synuclein.