All Signs Point to Tau Tangles as the Culprit in Fading Memory
Researchers at AAIC reinforced the idea that tau pathology drives cognitive decline, although amyloid plaques were implicated in semantic memory deficits.
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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.
Phase 1 clinical data presented at AAIC 2017 suggest few serious adverse events.
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.
Two new mouse studies show that a ketogenic diet that avoids obesity improves the health of mind and body, increasing median lifespan. Related studies hint at possible benefits for Alzheimer’s disease.
Engineering mice to express a tagged polyA-binding protein in specific cell types allows researchers to pull out neuronal, astroglial, or microglial mRNAs from the intact brain and examine each cell type′s mix of mRNA 3' ends.