Absent Aβ, Blood-Brain Barrier Breakdown Predicts Cognitive Impairment
A leaky blood-brain barrier in the hippocampus correlated with cognitive impairment, independently of other vascular risk factors or Alzheimer’s pathology.
NEWS
Could the Purported Muscle Exercise Hormone, Irisin, Jog Memory?
Levels of irisin are lower in brain and CSF of AD patients. Upping expression in mice protected them from synaptic deficits and memory problems.
First In Vivo Look at Amyloidosis Sparked by Dural Grafts
Researchers characterize widespread cerebral amyloid angiopathy and cortical plaques found in three living people who received dural grafts as children.
Secreted APP Binds GABA-B Receptors, Blocks Neurotransmitter Release
In presynapses, binding sequesters synaptic vesicles.
Tau, More than Aβ, Affects Sleep Early in Alzheimer’s
During deep sleep, people with AD pathology, particularly tau tangles, have less low-frequency slow-wave brain activity, which is important for memory consolidation.
Do Alzheimer’s Biomarkers Vary by Race?
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.
CryoEM γ-Secretase Structures Nail APP, Notch Binding
First look at substrate interactions reveals similarities but some surprises.
New PET Tracer Selectively Lights Up Activated Microglia in Brain
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.
Virtual Exhibit Hall
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome Dash Genomics, Inc. and Abcam, which join our other exhibitors — Biogen, BioLegend, BrainXell, NanoString Technologies, and the Jackson Laboratory.
SPOTLIGHT
Seeing Double: Two γ-secretase Structures Capture APP, Notch Binding
High-resolution cryoEM structures show that APP and Notch bind γ-secretase in broadly similar ways and that both undergo an identical molecular contortion that allows proteolysis. Nonetheless, subtle differences between the substrates may open the door to specific inhibitors of APP processing. The structures also reveal that AD mutations in presenilin and APP cluster at the enzyme-substrate interface, reinforcing the idea that altered APP processing causes AD.
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