In the United States, Racial Disparities in Dementia Risk Persist
Despite overall falling dementia rates in the U.S., black people remain more susceptible than whites.
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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.
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?
In the Alzheimer’s brain, too, plaques trigger a coordinated inflammatory response from microglia and astrocytes. A preprint paper had shown the same for mice.
At the at Tau2020 conference, scientists show high-resolution cryoEM of α-synuclein. Two different types of fibril are composed of asymmetric protofibril units.
In motor neurons of TMEM106b knockout mice, swollen vacuoles piled up in axons near the soma, rendering the mice wobbly and slow to react. The finding contradicts prior reports.
Different forms of p-tau in cerebrospinal fluid reflect worsening plaque load, metabolism, and atrophy in the brain. They could help stage Alzheimer’s disease.
P-tau217 appears sooner than p-tau181 in the brain, and it distinguishes AD from controls and other dementias even more cleanly.
For people with Parkinson’s, carrying Alzheimer’s genetic risk variants upped their odds of harboring Aβ and tau pathology and getting dementia. In people with DLB, Aβ plaques worsened tau and Lewy pathology, and cognition.