Could CD33 Be the Microglial Target for Stimulating Phagocytosis?
Inhibiting the receptor activates microglia to mop up debris, making CD33 an attractive therapeutic target.
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Inhibiting the receptor activates microglia to mop up debris, making CD33 an attractive therapeutic target.
Scientists are probing saliva and skin secretions for telltale signs of Parkinson’s disease. Their prize? A diagnostic test at the pre-motor stage.
In the largest study yet to track tau via repeated PET scans, researchers found that tau pathology increased over baseline only in people with Aβ deposition. The more tau a person had at baseline, the more tau increased later on, and the more they slipped on cognitive tests.
An FDA-approved insomnia drug lengthened total sleep time in patients with mild to moderate Alzheimer’s, suggesting it might be able to lessen a troublesome symptom of the disease.
More mouse data add to the argument that a flashing light sequence could potentially fight cognitive decline.
Lanabecestat, elenbecestat, and umibecestat all showed data at the AD/PD conference in Lisbon. Learn what definitely doesn’t work and what might yet.
Using single-nuclei or cell sorting, three separate research groups sequenced RNA from human postmortem brains. They unveiled AD-associated gene-expression signatures, but disease-related transcriptomes from human microglia were quite different from those in mice.
Thousands of stretches of the genome go undetected by standard short-read sequencing techniques. Unmasking these “dark regions” revealed a potential AD risk variant in the CR1 gene.
Scientists link this mysterious form of dementia to higher plasma LDL-cholesterol, and to genetic variants in APOB, which encodes the major component of low-density lipoprotein.
Organoids patterned on the dorsal human forebrain consistently contain a set of cells native to the cerebral cortex, and develop along the same trajectory as fetal brains. Could they become the standard for organoid research?
Serum from young mice boosted synapses and activity in human neurons. Researchers credit the proteins SPARCL1 and THBS4.
Researchers identify a specific SCF ligase that clears fibrillar but not physiologic forms of α-synuclein, suggesting potential for a targeted therapeutic approach.
In mice, inflammatory microglia must die, and new ones take over for efficient remyelination. Could problems with this changing of the guard contribute to neurological diseases?
As data increasingly blame the microglia response as a driving force in Alzheimer’s disease, researchers are investigating whether tempering these cells will aid cognition.
With three trials and initiatives to boost recruitment, GAP-Net is gaining some traction in the field.