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 cryo-EM 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.
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.
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.
The cells are primed to attack. Their targets include Epstein-Barr virus peptides.
An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.
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.
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.
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.
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.
Chemotherapy riles microglia, causing neurons to turn down expression of BDNF, a growth factor necessary for myelination. Restoring BDNF signaling on oligodendrocytes spared myelin and memory loss.
Analysis of a chimeric mouse shows that the cells express the same genes they do in the human brain, survey their environment, and respond to injuries and amyloid.