At AAIC, competitors vied for advantage, and discussion moved swiftly to the issue of assay standardization.
Greater lifetime estrogen exposure protects cognition, while hormone replacement therapy taken at menopause has no cognitive effects at all.
At AAIC, scientists said that alterations in how the aging female brain uses energy and metabolizes fat may leave APOE4 carriers particularly susceptible to tau pathology.
At AAIC, technology improves on pen-and-paper tests of early cognitive decline. Think learning Chinese, think smartphone burst, think digital clock.
A new PET tracer belies previous results from animal models and postmortem studies. Caveat emptor for trials of HDAC inhibitors?
Sensitive cognitive tests detect deficits in preclinical Alzheimer’s even before an amyloid scan reads positive. And CSF Aβ42 drops a decade before that—pushing research ever farther into the preclinical phase.
New data from gantenerumab and N3pG confirm that high-dose antibodies clear plaque dramatically, with manageable side effects. How will the aging brain respond?
A batch of new monoclonal antibodies against the C9ORF72 protein also revealed the protein lingers in presynapses.
A zinc-finger protein and a long noncoding RNA are now implicated in late-onset Alzheimer’s disease.
In early Parkinson’s disease, sparse areas on the retina correlate with dying dopaminergic neurons in the substantia nigra.
The drug, patisiran, targets messenger RNAs that cause transthyretin amyloidosis, a rare inherited neurodegenerative disease. Approval paves the way for other RNAi-based therapies.
Translatome profiling suggests ApoE drives a microglial gene-expression signature found in aging, Aβ amyloidosis, and tauopathy.
The acetylcholinesterase inhibitor failed to slow cognitive decline in people with both depression and mild cognitive impairment.
Data from the first human study hints the procedure could help deliver drugs to the brain, or even work as a therapy in its own right. A flurry of animal studies presented at AAIC support the idea.
In mice, aggregates of oxidized SOD1 accumulated with age, and endoplasmic reticulum stress made it worse. Does this explain SOD1 aggregates found in spinal cords of patients with sporadic ALS?