Presenilin-1 familial Alzheimer’s disease mutation alters hippocampal neurogenesis and memory function in CCL2 null mice
Copyright policy )Presenilin-1 familial Alzheimer’s disease mutation alters hippocampal neurogenesis and memory function in CCL2 null mice
Aberrations in hippocampal neurogenesis are associated with learning and memory, synaptic plasticity and neurodegeneration in Alzheimer's disease (AD). However, the linkage between them, β-amyloidosis and neuroinflammation is not well understood. To this end, we generated a mouse overexpressing familial AD (FAD) mutant human presenilin-1 (PS1) crossed with a knockout (KO) of the CC-chemokine ligand 2 (CCL2) gene. The PS1/CCL2KO mice developed robust age-dependent deficits in hippocampal neurogenesis associated with impairments in learning and memory, synaptic plasticity and long-term potentiation. Neurogliogenesis gene profiling supported β-amyloid independent pathways for FAD-associated deficits in hippocampal neurogenesis. We conclude that these PS1/CCL2KO mice are suitable for studies linking host genetics, immunity and hippocampal function.
- University of Nebraska Medical Center United States
Neurons, Endocrine and Autonomic Systems, Neurogenesis, Immunology, Long-Term Potentiation, Neurogliogenesis, Mice, Transgenic, Hippocampus, Behavioral Neuroscience, Disease Models, Animal, Mice, Chemokine, Alzheimer Disease, Mutation, Long-term potentiation, Presenilin-1, Animals, Humans, Maze Learning, Morris water maze, Chemokine CCL2
Neurons, Endocrine and Autonomic Systems, Neurogenesis, Immunology, Long-Term Potentiation, Neurogliogenesis, Mice, Transgenic, Hippocampus, Behavioral Neuroscience, Disease Models, Animal, Mice, Chemokine, Alzheimer Disease, Mutation, Long-term potentiation, Presenilin-1, Animals, Humans, Maze Learning, Morris water maze, Chemokine CCL2
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