Conditional genetic deletion of CSF1 receptor in microglia ameliorates the physiopathology of Alzheimer's disease

• Published in: Alzheimer's research & therapy Vol. 13; no. 1; p. 8
• Main Authors: Pons, Vincent, Lévesque, Pascal, Plante, Marie-Michèle, Rivest, Serge
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 05.01.2021; BioMed Central; BMC
• Subjects: Alzheimer Disease - genetics; Alzheimer's disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animal cognition; Animals; Antibodies; Binding sites; Bone marrow; Brain; Cognitive ability; Colony-stimulating factors (Physiology); Dementia; Development and progression; Disease Models, Animal; Gene expression; Genetic aspects; Health aspects; IL-34; Innate immunity; Kinases; Laboratories; mCSF; Membrane Glycoproteins - metabolism; Mice; Mice, Transgenic; Microglia; Mutation; Physiological aspects; Plaque, Amyloid; Prevention; Protein tyrosine kinase; Proteins; Receptor, Macrophage Colony-Stimulating Factor; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - genetics; Receptors, Immunologic - metabolism; Sheep; TREM2; Tumor necrosis factor-TNF; β-Catenin; Canada; Cognitive decline; Innate immunity; β-Catenin; Amyloid; TREM2; mCSF; IL-34; Phagocytosis; Microglia

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia in the world. Microglia are the innate immune cells of CNS; their proliferation, activation, and survival in pathologic and healthy brain have previously been shown to be highly dependent o...