David H. Allendorf

Cambridge, ENG, United Kingdom

Last Updated: 09/26/2026

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Found 12 publications

Correction to: Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer's disease.

Correction to: Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer's disease.

Journal: Acta neuropathologica

Published: February 15, 2023

Alzheimer's disease-associated R47H TREM2 increases, but wild-type TREM2 decreases, microglial phagocytosis of synaptosomes and neuronal loss.

Alzheimer's disease-associated R47H TREM2 increases, but wild-type TREM2 decreases, microglial phagocytosis of synaptosomes and neuronal loss.

Journal: Glia

Published: August 18, 2022

Neu1 Is Released From Activated Microglia, Stimulating Microglial Phagocytosis and Sensitizing Neurons to Glutamate.

Neu1 Is Released From Activated Microglia, Stimulating Microglial Phagocytosis and Sensitizing Neurons to Glutamate.

Journal: Frontiers in cellular neuroscience

Published: April 11, 2022

The microglial P2Y6 receptor mediates neuronal loss and memory deficits in neurodegeneration.

The microglial P2Y6 receptor mediates neuronal loss and memory deficits in neurodegeneration.

Journal: Cell reports

Published: April 16, 2021

Wild-type sTREM2 blocks Aβ aggregation and neurotoxicity, but the Alzheimer's R47H mutant increases Aβ aggregation.

Wild-type sTREM2 blocks Aβ aggregation and neurotoxicity, but the Alzheimer's R47H mutant increases Aβ aggregation.

Journal: The Journal of biological chemistry

Published: February 05, 2021

Microglial phagocytosis of neurons in neurodegeneration, and its regulation.

Microglial phagocytosis of neurons in neurodegeneration, and its regulation.

Journal: Journal of neurochemistry

Published: October 02, 2020

Sialylation acts as a checkpoint for innate immune responses in the central nervous system.

Sialylation acts as a checkpoint for innate immune responses in the central nervous system.

Journal: Glia

Published: August 31, 2020

Sialylation and Galectin-3 in Microglia-Mediated Neuroinflammation and Neurodegeneration.

Sialylation and Galectin-3 in Microglia-Mediated Neuroinflammation and Neurodegeneration.

Journal: Frontiers in cellular neuroscience

Published: March 29, 2020

Lipopolysaccharide activates microglia via neuraminidase 1 desialylation of Toll-like Receptor 4.

Lipopolysaccharide activates microglia via neuraminidase 1 desialylation of Toll-like Receptor 4.

Journal: Journal of neurochemistry

Published: January 15, 2020

Activated microglia desialylate their surface, stimulating complement receptor 3-mediated phagocytosis of neurons.

Activated microglia desialylate their surface, stimulating complement receptor 3-mediated phagocytosis of neurons.

Journal: Glia

Published: September 23, 2019

Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer's disease.

Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer's disease.

Journal: Acta neuropathologica

Published: November 23, 2018

Activated Microglia Desialylate and Phagocytose Cells via Neuraminidase, Galectin-3, and Mer Tyrosine Kinase.

Activated Microglia Desialylate and Phagocytose Cells via Neuraminidase, Galectin-3, and Mer Tyrosine Kinase.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Published: December 03, 2015

Showing 1-12 of 12

Last Updated: 09/26/2026