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Deciphering neutrophil dynamics: Enhanced phagocytosis of elastic particles and impact on vascular-targeted carrier performance.
Sci Adv
January 2025
Department of Chemical Engineering, University of Michigan, Ann Arbor, MI 48109, USA.
Particle elasticity has widely been established to substantially influence immune cell clearance and circulation time of vascular-targeted carriers (VTCs). However, prior studies have primarily investigated interactions with macrophages, monocytic cell lines, and in vivo murine models. Interactions between particles and human neutrophils remain largely unexplored, although they represent a critical aspect of VTC performance.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Michigan, Ann Arbor, MI, USA.
Background: Alzheimer's disease (AD) is the leading cause of dementia worldwide. The recent announcement that lecanemab, a monoclonal antibody targeting amyloid-b, can slow down cognitive decline in AD is a great step forward in the battle against the disease. However, the modest success achieved in the clinical trial speak to the need for developing additional pharmaceutical approaches to target other key features of AD.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Washington University School of Medicine, Saint Louis, MO, USA.
Background: A recent case report described an individual who was a homozygous carrier of the APOE3 Christchurch (APOE3ch) mutation and resistant to autosomal dominant Alzheimer's Disease (AD) caused by a PSEN1-E280A mutation. Whether APOE3ch contributed to the protective effect remains unclear.
Method: We generated a humanized APOE3ch knock-in mouse and crossed it to an amyloid-β (Aβ) plaque-depositing model.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Denali Therapeutics Inc., South San Francisco, CA, USA.
Background: Macrophages and microglia are myeloid cells that play critical roles in the surveillance of the local environment of the tissues in which they reside. The ability of these phagocytes to perform key functions is contingent on their capacity to sense extracellular cues and mount responses that involve chemotaxis, proliferation, cytokine secretion, and phagocytosis of various cargos for lysosomal clearance. Our overarching hypothesis is that lysosomal degradation of phagocytic cargoes is critical for the resolution of cellular/tissue damage, as well as of inflammation, and that failure to accomplish this step affects myeloid cell states and immune responses.
View Article and Find Full Text PDFBackground: Microglia are the primary immune cells of the brain and represent the main line of defense against brain environmental insults. In recent years, microglia have been implicated in Alzheimer's disease (AD) pathogenesis by having interconnected yet opposing roles: beneficial as they clear amyloid beta (Aβ) and amyloid plaques, and detrimental as being responsible for synaptic and neuronal loss. These activities are tightly regulated by microglia receptors CD33 and TREM2.
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