| First Author | Poirier GL | Year | 2011 |
| Journal | Neuroscience | Volume | 174 |
| Pages | 71-83 | PubMed ID | 21093545 |
| Mgi Jnum | J:170261 | Mgi Id | MGI:4946154 |
| Doi | 10.1016/j.neuroscience.2010.11.025 | Citation | Poirier GL, et al. (2011) Early-onset dysfunction of retrosplenial cortex precedes overt amyloid plaque formation in Tg2576 mice. Neuroscience 174:71-83 |
| abstractText | A mouse model of amyloid pathology was used to first examine using a cross sectional design changes in retrosplenial cortex activity in transgenic mice aged 5, 11, 17, and 23 months. Attention focused on: (1) overt amyloid labeled with beta-amyloid((1-42)) and Congo Red staining, (2) metabolic function assessed by the enzyme, cytochrome oxidase, and (3) neuronal activity as assessed indirectly by the immediate-early gene (IEG), c-Fos. Changes in cytochrome oxidase and c-Fos activity were observed in the retrosplenial cortex in Tg2576 mice as early as 5 months of age, long before evidence of plaque formation. Subsequent analyses concentrating on this early dysfunction revealed at 5 months pervasive, amyloid precursor protein (APP)-derived peptide accumulation in the retrosplenial cortex and selective afferents (anterior thalamus, hippocampus), which was associated with the observed c-Fos hyporeactivity. These findings indicate that retrosplenial cortex dysfunction occurs during early stages of amyloid production in Tg2576 mice and may contribute to cognitive dysfunction. |
