How Does COVID-19 Affect the Brain?
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?
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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.
The more a person’s gut microbiome becomes individualized with age, the longer that person's lifespan and the better his or her health, say scientists.
In early stage trials, light and sound promoted neuronal communication, calmed immune cells, and slowed brain atrophy, but cognitive benefit remains unclear.
Award recognizes discoveries of genetic variants that perturb liquid-liquid phase separation and increase risk for ALS-FTD and other neurodegenerative diseases.
Avid’s postmortem validation data indicate Alzheimer’s can be diagnosed by visual examination of flortaucipir PET scans.
In stark contrast to Aβ and tau fibrils, α-synuclein fibrils are asymmetric, comprising two different protofibrils.
Umbilical cord stem cells from presenilin 1 E280A carriers, once differentiated into cholinergic-like neurons, pumped out Aβ42 and accumulated phosphorylated tau and apoptotic markers.
Induced neurons lacking the Alzheimer’s risk gene can’t properly recycle APP.
In cell culture, slashing Aβ production by more than half harmed neuronal signaling, but a smaller cut maintained it.
New research suggests the R47H variant protects neurons from neurodegeneration, raising questions about staging and direction of future TREM2-based therapy.
By suppressing a single gene, scientists triggered the transformation of astrocytes into neurons in the mouse substantia nigra, where the converts released dopamine and connected with the striatum.
A mouse study claims that the small GTPase restrains pro-inflammatory responses in microglia. Aβ oligomers inhibit RhoA, promoting Aβ deposition and neurodegeneration.
Released from hippocampal neurons in response to experience, the cytokine prompted microglia to eat extracellular matrix around synapses. This facilitated growth of new spines, and sharpened memory.
This early marker distinguishes Alzheimer’s from controls and other neurodegenerative diseases more accurately than other biomarkers.