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.
NEWS
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.
In Alzheimer’s, Too Little REST Spurs Too Much Neurogenesis
Neural progenitor cells derived from people with sporadic AD are missing the transcriptional repressor REST in the nucleus. This lets neurogenesis run wild, exhausting a person’s stem cell pool.
ApoE Binds Complement Protein, Keeps Inflammatory Cascade in Check
Binding occurs around lipid deposits in the choroid plexus, near Aβ deposits, and also in atherosclerotic plaques in blood vessels.
In Pathology Cascade, Microglia Rev Up After Plaques but Before Tangles
Amyloid plaques in postmortem human cortex correlated with the proportion of microglia that were activated, not with microglial numbers. Tau pathology and cognitive decline come later.
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.
Cancer Treatment Takes Aim at Tauopathy
Are checkpoint inhibitors—FDA-approved anti-cancer immunomodulators—heading to clinical trials for the treatment of Alzheimer’s? Two years ago, studies suggested these therapeutic antibodies cleared amyloid and improved memory in the 5xFAD mouse model. Now, the same scientists report the strategy also works on different transgenic mice modeling tauopathy. Other groups are skeptical, and point to problems replicating the original data.
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