| First Author | Kiyota T | Year | 2015 |
| Journal | Brain Behav Immun | Volume | 49 |
| Pages | 311-21 | PubMed ID | 26112421 |
| Mgi Jnum | J:329602 | Mgi Id | MGI:6832135 |
| Doi | 10.1016/j.bbi.2015.06.014 | Citation | Kiyota T, et al. (2015) Presenilin-1 familial Alzheimer's disease mutation alters hippocampal neurogenesis and memory function in CCL2 null mice. Brain Behav Immun 49:311-21 |
| abstractText | Aberrations in hippocampal neurogenesis are associated with learning and memory, synaptic plasticity and neurodegeneration in Alzheimer's disease (AD). However, the linkage between them, beta-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 beta-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. |
