Adenosine Receptors Rev Up Immune Response, Memory Loss, in Tau Model
Overexpressing neuronal A2A receptors stoked C1q in microglia, damaging synapses and memory.
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Overexpressing neuronal A2A receptors stoked C1q in microglia, damaging synapses and memory.
Ablating the immune cells protected mouse models of frontotemporal dementia from the neurodegeneration caused by human ApoE4.
The first ever cryoEM structures of Aβ fibrils extracted from AD tissue look quite different than prior structures of fibrils generated in vitro. For starters, they are right-hand twisted, not left-hand.
Imaging studies suggest that ApoE4 carriers may be more susceptible to the effects of tangles, particularly if they are women.
The cells are primed to attack. Their targets include Epstein-Barr virus peptides.
Aβ oligomers latch onto adrenergic receptors, mobilizing a kinase that phosphorylates tau. Blocking adrenergic signaling wards off memory problems in amyloidosis mice.
Functional connections between two brain regions are the strongest indicator that pathologic, accumulated tau will spread from one to another.
Two studies reveal new aspects of the neurovascular physiology that regulate the flow of oxygenated blood into the brain’s arterioles and capillaries in response to neuronal stimulation.
Under diabetic conditions, SERP1 binds secretase subunit, cranking up cleavage of APP but not Notch. The finding offers a mechanistic link between diabetes and Alzheimer’s.
Eliminating microglia in a mouse model of amyloidosis nearly abolished parenchymal plaques, but led to a huge buildup of amyloid in cerebral blood vessels.
Sedentary mice infused with the plasma of active ones had more newborn neurons in the brain and less neuroinflammation. Exercising upped plasma clusterin in mice and in humans.
Blocking the receptor clears toxic proteins and improves memory in old mice. The work proposes a new role in microglia for a well-known B-cell receptor.
Microglia cleanup, mitophagy, axonal plasticity, blood-brain barrier. A renewed focus on ApoE4 is revealing new ways in which this isoform renders the brain vulnerable to Alzheimer’s.
In a research study, one-fifth of healthy people who learned they were at high risk for AD said they might consider physician-assisted death as a future option.
“We are learning” was the tenor of debate about the latest round of setbacks for anti-amyloid trials in symptomatic Alzheimer’s disease at a recent conference in Lisbon.