This year, the AAIC conference showcased a field that is doggedly inching toward an effective anti-amyloid therapy while at the same time branching out from its usual ways of doing things. The antibody BAN2401 showed promising Phase 2 data, making it the latest in a handful of such therapeutics shown to robustly remove brain amyloid. (Hint: Crank the dose.) A fifth antibody, crenezumab, might remove CSF Aβ oligomers, a long-elusive species the field finally appears able to measure. Other scientists showed progress on capturing the decades-long disease process in deeper ways. They include measuring brain amyloid by way of a blood test, detecting neurodegeneration by way of blood neurofilament light protein levels, imaging synapses and—last but not least—new tests that catch subtle subtle cognitive deficits many years prior to the overt forgetting that used to be called symptom onset. (Hint: tau.) Non-amyloid-centered research is growing apace, supporting large initiatives to study the cardiovascular components of dementia, metabolic underpinnings of sex differences in AD, innovative drug-delivery approaches using ultrasound, and tech-based ways to support research and patient care.
Researchers consider the data encouraging, though questions linger about the cognition results. Did regulators mess up the randomization of this trial?
Analyzing Phase 2 trial CSF of an investigational immunotherapy, scientists showed for the first time that treatment mitigates neurotoxic oligomers in patients.
UCB-J hints at early synaptic loss in the hippocampus, but not the cortex. Researchers puzzle over the pattern.
In SPRINT MIND trial, strict control of systolic pressure slashed MCI incidence by almost 20 percent.
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.
New data from gantenerumab and N3pG confirm that high-dose antibodies clear plaque dramatically, with manageable side effects. How will the aging brain respond?
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.
A new PET tracer belies previous results from animal models and postmortem studies. Caveat emptor for trials of HDAC inhibitors?
At AAIC, technology improves on pen-and-paper tests of early cognitive decline. Think learning Chinese, think smartphone burst, think digital clock.
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.
Greater lifetime estrogen exposure protects cognition, while hormone replacement therapy taken at menopause has no cognitive effects at all.
At AAIC, competitors vied for advantage, and discussion moved swiftly to the issue of assay standardization.
Data from two independent cohorts suggest that the risk to the brain from high blood pressure and cardiovascular disease begins in a person’s 40s or before.
With buckets of new data at AAIC, blood NfL grabbed attention as a telltale of neurodegeneration. The protein predicts progression, and might one day track treatment effects.
What's the use of measuring neurofilament light in blood? The marker could help with AD trial enrollment and measuring drug effects. It could even guide brain-sparing improvements in heart surgery, say researchers at AAIC 18.
AAIC showcased advances in scientists’ attempts to integrate technology into dementia care and research. This includes the use of furry robot seals to keep patients company.