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.
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.
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.
Much of the neuron loss in rTg4510 mice comes from accidental disruptions in mouse genes rather than expression of mutant tau. Pathology spreads quickly in human tau knock-ins.
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.
Resident T cells in the membrane surrounding the healthy mouse brain influence both short-term memory and synaptic plasticity.