In Mice, Aducanumab Neutralizes Aβ Seeds
Could this forestall the amyloid cascade and the onset of Alzheimer’s disease?
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Could this forestall the amyloid cascade and the onset of Alzheimer’s disease?
Despite overall falling dementia rates in the U.S., black people remain more susceptible than whites.
Neurons take up extracellular vesicles containing tau oligomers more readily than they do free tau. Some gift: This speeds the march of tauopathy through mouse brain.
In both mice and (wo)men, the sex difference comes down to an Aβ-glutamate receptor-prion protein troika.
High amyloid burden and neuroinflammation, neuronal excitability, and tangles and oligodendrocyte loss distinguish the disease types.
The blood-based marker may be far more scalable and cost-effective for tracking the disease than PET imaging and CSF biomarkers.
By tracing the transcriptomes of neurons that wither early and late in the course of Alzheimer’s disease, researchers peg subpopulations of excitatory neurons in entorhinal cortex as selectively vulnerable to tau. Reactive astrocytes aid and abet.
Aging macrophages and microglia poorly burn glucose and enter an inflammatory state. Revving their metabolism preserved synapses and memory in mice. What does prostaglandin have to do with it?
By looking for SNPs that affect how transcription factors bind DNA, researchers nominated causal genes for 30 Alzheimer’s and Parkinson’s GWAS hits.
In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
By pinpointing where tau pathology starts in a person’s brain, researchers better predicted future spread and determined small changes in tangle load.
Amyloids of AIMP2 found in Parkinson’s disease may seed α-synuclein aggregation.
Among a growing number of blood-based tauopathy markers, this new immunoassay may offer a way to catch preclinical disease just before symptoms show up.
In mice, forebrain neurons with hobbled retromers ooze fragments of tau and several BACE1 substrates into the CSF. Similar proteins are up in CSF from people with MCI and Alzheimer’s disease.
This astrocytic glycoprotein greases glial phagocytosis and reduces plaque burden in mice. The circadian clock protein Bmal1 suppresses it.