Pseudotime Simulates Disease Progression from Case-Control RNA-Seq
Aligning single-cell gene expression in “pseudotime” models longitudinal change. It explores how healthy cells become sick during Alzheimer's.
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Aligning single-cell gene expression in “pseudotime” models longitudinal change. It explores how healthy cells become sick during Alzheimer's.
Three new papers report these myelin-producing cells contribute up to a third of plaque Aβ in transgenic mice.
New data from gantenerumab and N3pG confirm that high-dose antibodies clear plaque dramatically, with manageable side effects. How will the aging brain respond?
With several thousand people across the U.S. on the drug, wait times are long, and clinics are hiring. How to meet growing demand?
By consensus, leaders in the astrocyte and microglia fields recommend that investigators eschew names in favor of detailed descriptions of reactive glia, with a focus on functional changes.
Lipids, amino acids, carbohydrates, and other molecules in the CNS linked to genetic variants, some of which upped the risk for neurodegenerative disease.
A Tolstoy-inspired method identifies AD variants that exert similar effects, pinpointing causal AD proteins—six known, plus a new one, RET.
With age, this coupling erodes, making synapses sluggish. Rekindling it lessens synaptic deficits and memory loss in old mice.
In mice, the long noncoding RNA MEG3 mediated the death of human neurons, which accumulated tau tangles.
By tracking how mutations influence the incorporation of monomers, scientists pinpoint which residues shape tau fibrils.
In AD mouse models, replacing ApoE3 with ApoE3Ch preserves memory.
ARF Scientific Advisor David Holtzman, of Washington University, St. Louis, Missouri, sent us this report from the IPSEN Foundation conference "Immunization against Alzheimer's and other Neurodegenerative Diseases," held on 13 March in Paris, France...
Plaque clearance is a better correlate of neural protection via passive amyloid immunization than soluble amyloid-beta (Aβ) clearance, and this protection is based on Fc receptor-mediated Aβ phagocytosis...
Thomas Wisniewski, Einar Sigurdsson, and colleagues at New York University report that they have prevented amyloid-β deposition by immunizing a mouse model of Alzheimer's disease with a nontoxic Aβ homologue...
Crumbling microtubules, those slender filaments that aid a variety of cellular processes from cell division to vesicle trafficking, could lead to motor neuron disease...
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