Huang Y, Lemke G.
Early death in a mouse model of Alzheimer's disease exacerbated by microglial loss of TAM receptor signaling.
Proc Natl Acad Sci U S A. 2022 Oct 11;119(41):e2204306119. Epub 2022 Oct 3
PubMed.
In the absence of the TAM receptor Mer or its ligand Gas6, excess excitatory synapses in the hippocampus—between the dentate gyrus (DG) and target neurons in the CA3 field—are generated. This is because excess neurons in the DG are not eliminated by Mer-dependent microglial "phagoptosis." The excess excitatory connections greatly exacerbate the incidence of lethal seizures seen in the APP/PS1 mouse model of Alzheimer's disease.
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Salk Institute
In the absence of the TAM receptor Mer or its ligand Gas6, excess excitatory synapses in the hippocampus—between the dentate gyrus (DG) and target neurons in the CA3 field—are generated. This is because excess neurons in the DG are not eliminated by Mer-dependent microglial "phagoptosis." The excess excitatory connections greatly exacerbate the incidence of lethal seizures seen in the APP/PS1 mouse model of Alzheimer's disease.
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