Blocking the microglial receptor for pro-inflammatory prostaglandin D2 protects motor neurons from glial toxicity in ALS cell and mouse models.
The overused adage of the fountain of youth rears its head again, as four new studies show how young blood rejuvenates old brain and muscle, pumping up the vasculature, stem cells, and restoring microglia’s appetite for waste products. Researcher are isolating the responsible factors, for example GDF11.
By finding differences in gene expression between monocytes and T cells, scientists reveal that the innate immune system has strong ties to neurodegenerative disease.
A small molecule inhibitor kills all microglia in the brain, but the cells rapidly repopulate from a previously unidentified progenitor cell.
The scientific spotlight often shines on excitatory neurons as the brain’s main Aβ factories. What about other cell types?
Already linked to Alzheimer’s and other neurodegenerative diseases, a TREM2 variant now shows up on the ALS radar, too.
Neuroligin, a synapse-building protein previously tied to autism, may play a part in Alzheimer’s disease through neuroinflammation and DNA transcription.
Scientists are tweaking immune pathways to scavenge amyloid and curb symptoms in Alzheimer’s mice.
Presented at CTAD, BACE inhibitor’s efficacy and safety results in mild to moderate AD were encouraging to some clinicians, vaguely disquieting to others.
New research reveals fundamental roles for astrocytes and microglia in shaping neural circuits.
Without the protein beclin 1, rapacious microglia choke on amyloid β.
Researchers identified a genetic variant in the microglial gene CD33 that protects against Alzheimer’s.
Researchers identify the Aβ-binding scavenger receptor CD36 as a key regulator of macrophage inflammasome responses...
Growing evidence suggests that innate immune cells prevent or slow Alzheimer's disease by chewing up Aβ and promoting its clearance.
Could amyloid-beta fibrils—which form the hallmark plaques of Alzheimer’s disease (AD)—actually protect the brain?...
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