Immune Cells Clog Capillaries in Mice, Disrupt Memory
In mouse models of Alzheimer’s, neutrophils stick to capillaries in the cerebral cortex, reducing blood flow. Keeping those cells moving or depleting them altogether improved memory.
NEWS
Studies Point to DNA Difficulties in ALS/FTD
New work implicates changes in chromatin structure and failed DNA repair in neurodegeneration.
Could Disposing of Damaged Mitochondria Treat Alzheimer’s Disease?
In several animal models, stimulating mitophagy lowered amyloid deposits and tau phosphorylation while improving learning and memory.
Clotting Protein from Blood Incites Microglia, and Synapses Die
When it seeps into the brain, fibrinogen activates innate immune responses that zap dendrites. And amyloid deposition has little to do with it.
Is a Woman’s Brain More Susceptible to Tau Pathology?
Among cognitively normal people with amyloid plaques, women have more tau tangles in the entorhinal cortex than do men. Does this indicate susceptibility, or resilience?
Panel of Blood Markers Signals Amyloid in Brain
In cognitively normal people, a set of blood proteins may predict whether or not amyloid plaques have deposited in a person’s brain.
Cholesteryl Esters Hobble Proteasomes, Increase p-Tau
Reducing these esters with statins and cholesterol-hydroxylase-activating drugs lowers phospho-tau and Aβ in neurons. One such drug is approved to treat HIV AIDS.
Cancer Treatment Takes Aim at Tauopathy
Building on results in AD mouse models, researchers now report that immune checkpoint inhibitors reduce pathology and improve cognition in tauopathy mice, too. Other scientists are skeptical.
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
Clotting Protein from Blood Incites Microglia, and Synapses Die
Blood leaks in the brain increase the risk for Alzheimer’s disease and dementia, and a new study suggests that immune responses to blood-clotting proteins are to blame. In a mouse model of amyloid deposition, fibrinogen that entered the brain activated microglia, leading to synaptic pruning. The process does not require Aβ, because fibrin foci devoid of amyloid induced neurite dystrophy. Preventing fibrinogen from binding microglia improved learning and memory in the mice, suggesting a possible new avenue for dementia treatment.
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