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?
In response to an FDA request, the drug’s sponsor submitted new data analyses. The agency moved the action date to June 7.
The commercial test uses a few drops of saliva. It must be ordered by a physician. Plans are also in the works to use the test to select participants for clinical trials.
White matter-associated microglia express similar genes to plaque-associated DAMs. They seem to be triggered by the myelin breakdown associated with aging and disease.
Already implicated in dementia, this lysosomal receptor appears to play a role in the development of COVID-19.
In the negative Phase 2 trial of prasinezumab, populations with more rapid decline benefited; this informed the design of a new Phase 2b study.
Data from Phase 3 trials of elenbecestat show no harm to cognition, leaving open a chance that the drugs could be used safely in the future.
Some people with severe COVID-19 have neurovascular injury and elevated markers of neural damage in their blood and CSF. What’s going on in their brains?