Necroptosis Rampant in the Alzheimer’s Brain?
Markers of necroptosis peppered postmortem brain tissue from people with AD. Gene expression implicates RIP kinases. Could shuttering this cell death pathway save neurons?
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Markers of necroptosis peppered postmortem brain tissue from people with AD. Gene expression implicates RIP kinases. Could shuttering this cell death pathway save neurons?
One report implicates APP’s intracellular domain in neuron loss due to LRRK2; another accuses the AICD fragment of regulating mitochondrial dynamics via Pink-1.
FUS proteins tend to link up and form liquid droplets and, from those, aggregates. Phosphorylation of the protein’s low-complexity domain repels these associations.
High-throughput sequencing yields surprises. Learn about pathogenic variants in endosomal genes, an algorithm to nab the worst SORL1 mutations, dominant PS1 mutations arising de novo, and tau duplications.
Researchers at AAIC reinforced the idea that tau pathology drives cognitive decline, although amyloid plaques were implicated in semantic memory deficits.
Researchers at AAIC described different correlates of CSF and PET measures of Aβ and tau.
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.
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.
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.
AAIC presentations identified early imaging changes in aging and AD, and reinforced the idea that CSF markers change little over the short term.
Tamping down a cell stress response saves neurons from degenerating while helping mice retain both their strength and their wits.
Hsp90, a protein chaperone that helps misfold tau, enlists the co-chaperone Aha1 in the process. Could crippling Aha1 reduce tau aggregation?
Researchers at AAIC presented several imaging measures that may help explain the phenomenon of preserved cognition in the face of AD pathology.
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.
Three BACE inhibitors, a γ-secretase modulator, and a phosphodiesterase inhibitor appeared safe in Phase 1 trials.
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