A Facial Massage May Get the CSF Flowing
Manipulation of lymph vessels in the face and neck boosts cerebrospinal fluid drainage in old mice
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Manipulation of lymph vessels in the face and neck boosts cerebrospinal fluid drainage in old mice
As mice age, monocyte-derived macrophages settle in their nigrostriatal region and become bona fide microglia. Cells with hematopoiesis mutations can impair movement.
Fetal liver monocytes were the only kind that developed a true microglia identity in mouse brains. A clue? Their chromatin structure at the Sall1 locus.
Transplanting healthy macrophages into a Krabbe mouse model erased the disease’s giant toxic cells, reduced pathology, and lengthened survival.
The device identified people with this disease in a small pilot study.
In a mouse model of AD, the membrane repair protein annexin A6 reduced dystrophic neurites and tau phosphorylation.
In tauopathy mice, an orexin receptor antagonist keeps the brain from wasting away.
Deleting the kinase PERK in astrocytes, or blocking it, restored glymphatic flow in the brains of AD mice, improving cognition and protein clearance.
Bespoke enhancers refine gene expression in both neural and non-neural cells of the central nervous system.
A high concentration of TDP-43 and a wave of oxidative stress drive protein phase transitions within the membraneless organelles.
When the catecholamine binds adrenergic receptors on astrocytes, the glia release neuromodulators that tweak the strength of neuronal synapses.
The transmembrane protein forms a complex with Aβ, which is then degraded with help from LRP1.
In amyloidosis mice, a dearth of NPTX2 in layer 5/6 excitatory neurons quiets interneurons, dampening inhibitory signals. Adding NPTX2 restores them.
In mice, plaque-coated vessels shed extracellular vesicles that infiltrate the brain and exacerbate ischemic damage.
Donor-derived brain tissue and cells are helping scientists decipher the molecular pathology of human tauopathies.
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