Peter Davies, Beloved Giant of Alzheimer’s Disease Research, Dies at 72
In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
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In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
Most observational cohorts are on pause, and many clinical trials have stopped dosing. The long-term effects on the integrity of AD studies are unclear.
While the FDA weighs aducanumab’s marketing license application, Alzheimer’s researchers agree that the agency’s own statistician correctly assessed the data as weak. Most prefer that one more trial be done.
DIAN, Roche, Lilly disclose that neither gantenerumab nor solanezumab slowed cognitive decline in the first-pass comparison of drug and placebo groups. Analyses are ongoing; dose may have been too low.
A panel of experts concludes the evidence for this scary prospect is weak, but recommends neurosurgeons use separate neurosurgical instruments for young and old patients. The experts called for further studies.
Researchers implicate PrP in the toxicity of Aβ, tau, and α-synuclein oligomers in several neurodegenerative diseases.
A survey of 16 purported conformation-specific antibodies found that most bound nearly equally well to oligomers and fibrils, and weakly to monomers.
A large multinational epidemiology study finds only small and inconsistent associations.
Acting downstream of TREM2, PLCγ2 facilitates phagocytic microglial behavior such as lipid processing. PLCγ2 also acts downstream of toll-like receptors, where it can throw a switch to inflammation.
Cognitive enrichment in early life correlated with less Alzheimer’s pathology, and slower cognitive decline, in late life.
Overexpressing the endosomal activator in neurons not only caused those organelles to swell, but also bungled synaptic transmission, goaded hyperphosphorylation of tau, and destroyed cholinergic neurons.
A postmortem study found that people who had more aggregation-prone, hyperphosphorylated, oligomeric forms of tau in their brains also had a more aggressive form of Alzheimer’s disease during life. Will we personalize tauopathy care like cancer care?
Middle-aged WTC responders have cognitive problems, which correlate not only with their PTSD symptoms and exposure to toxic dust, but also with biomarkers of amyloid and tau.
In the human brain, alpha waves fell out of sync, while delta-theta waves swelled in concert with amyloid plaques, neurofibrillary tangles. Alpha modulation correlated with cognitive decline.
In female mice it’s the other X chromosome, not lack of a Y, that extends life and preserves memory in the face of amyloidosis. A histone demethylase gene partly explains this. It protects people, too.