At AAIC, secondary endpoint data from the API Colombian study showed trends favoring crenezumab, while people taking gantenerumab in open-label extensions declined more slowly than matched controls.
At AAIC, and a separate BACE symposium, scientists argued the case for resuming evaluation of these drugs in clinical trials.
New technology identified a rare population of astrocytes around blood vessels and hundreds of plaque-associated genes.
Finally, blood biomarkers for AD are here. Alas, the path to routine use is fraught. At AAIC, scientists discussed new guidelines, head-to-head comparisons, and logistical, technical, and ethical hurdles ahead.
A cast of blood biomarkers for Alzheimer's has emerged from studies in research cohorts, and is now being put to the test in community cohorts. At AAIC, direct comparisons of top contenders showed that some detect amyloid and impending cognitive decline.
Certain blood biomarker tests can tell that amyloid has built up in a person's brain and that their thinking will decline. What are the challenges ahead before these tests can be rolled out to medical care settings everywhere?
Rare AD risk variants cluster within TREM2, SORL1, and the newcomer EXOC3L4. Rare mutations in ABCA7 associate with cerebral amyloid angiopathy.
A mathematical model predicts that a tiny difference in CDR-SB after two years of treatment would grow fivefold over the next three years as progression curves separate.
Scientists are refining safety and biomarker disclosure protocols, and are preparing to collect data on how well the new drugs work.
In “Maintain Your Brain,” virtual interventions gave participants a memory boost. In EXERT, cognition held steady in people who exercised. Both groups were coached.
The I-CONECT trial found that regular video chats boosted cognition in socially isolated older people. Even a weekly phone call enhanced their feelings of social connectedness.
Plasma p-tau217 and p-tau181 better track amyloid PET, tangles, and subtle cognitive decline.
The autopsy of a woman with a the PSEN1 Paisa mutation plus a homozygous ApoE3 variant showed an unusual distribution of tau tangles. Gene-expression studies pinpointed vulnerable neurons that were spared, and riled-up microglia in tangle-ridden zones.
In a large European study, the scans changed the diagnosis in a third of cases. They boosted the doctor's confidence in making the call, and predicted cognitive decline.
Soluble p-tau, aggregation epicenters, and gene variants emerged as potential forces that might influence how quickly tangles propagate through the brain.
Microglial ApoE4 hobbled these cells' protective responses against Aβ and tau. In the meninges, ApoE4 made by myeloid cells slowed lymphatic drainage; at the blood-brain barrier, ApoE4 steered aging endothelial cells and pericytes toward dysregulation.
Analysis identified neuronal populations that die early in AD and glial subtypes that expand. Gliosis signaled fast memory decline.
By pooling single-nucleus RNA-sequencing datasets, scientists found consistent changes across Alzheimer’s cohorts. Examples: hypermetabolic transcription, and a new neuron population that dies early on.
Aligning single-cell gene expression in “pseudotime” models longitudinal change. It explores how healthy cells become sick during Alzheimer's.