Loss of Pericytes Wreaks Havoc in Mouse Brain
Knocking down these capillary-hugging cells triggers a domino effect; blood proteins invade the brain, white matter deteriorates, and neurons die.
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Knocking down these capillary-hugging cells triggers a domino effect; blood proteins invade the brain, white matter deteriorates, and neurons die.
Two different model systems catalogued cell states: DAM-like, antigen-presenting, cytokine-, and interferon-based. More work is needed to pin down function.
In the field's quest for disease-modifying treatments, two different α-synuclein vaccines and two antibodies look promising in preclinical studies, as well.
With effective symptomatic treatments in hand, many Parkinson’s researchers have now set their sights on loftier goals...
Alzheimer’s researchers got their first look at data from the positive Phase 3 trial. Many expect this antibody to become the third approved immunotherapy for AD.
At AD/PD, scientists presented small molecules that break up fibrils and antibodies that target pathogenic forms of α-synuclein or hinder spread in iPSCs and mice.
New findings shed light on the intracellular processes that dictate tau seeding inside and between cells, and which forms are toxic to neurons.
The panel was persuaded of the antibody’s clinical efficacy and overall favorable benefit/risk ratio, although it had questions about risk in certain subgroups.
By interfering with Aβ fibril growth, prion and two other cell-surface proteins may drive production of smaller, more toxic, oligomers and protofibrils.
In a mouse amyloidosis model, a protective variant tightened the reins on plaques and spared synapses; a risk variant did the opposite.
An antibody against the inhibitory receptor LILRB4 prevented its binding to ApoE. The upshot? Microglia engulfed more Aβ fibrils and plaque load fell.
Reactive astrocytes spell trouble for synapses, while microglial transform from protective to destructive as disease progresses.
The addition of SUMO2 to tau prevents its phosphorylation and aggregation, preserving synapses and memory in tauopathy mouse models.
In a small dose-finding study, Roche’s new brain-shuttle-based anti-amyloid antibody mopped up nearly all plaques in three months, without triggering edema.
For a diagnostic test, specificity and sensitivity fall a little shy. Using two cut points might solve the problem.
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