| First Author | Harris JA | Year | 2010 |
| Journal | Neuron | Volume | 68 |
| Issue | 3 | Pages | 428-41 |
| PubMed ID | 21040845 | Mgi Jnum | J:167860 |
| Mgi Id | MGI:4880823 | Doi | 10.1016/j.neuron.2010.10.020 |
| Citation | Harris JA, et al. (2010) Transsynaptic progression of amyloid-beta-induced neuronal dysfunction within the entorhinal-hippocampal network. Neuron 68(3):428-41 |
| abstractText | The entorhinal cortex (EC) is one of the earliest affected, most vulnerable brain regions in Alzheimer's disease (AD), which is associated with amyloid-beta (Abeta) accumulation in many brain areas. Selective overexpression of mutant amyloid precursor protein (APP) predominantly in layer II/III neurons of the EC caused cognitive and behavioral abnormalities characteristic of mouse models with widespread neuronal APP overexpression, including hyperactivity, disinhibition, and spatial learning and memory deficits. APP/Abeta overexpression in the EC elicited abnormalities in synaptic functions and activity-related molecules in the dentate gyrus and CA1 and epileptiform activity in parietal cortex. Soluble Abeta was observed in the dentate gyrus, and Abeta deposits in the hippocampus were localized to perforant pathway terminal fields. Thus, APP/Abeta expression in EC neurons causes transsynaptic deficits that could initiate the cortical-hippocampal network dysfunction in mouse models and human patients with AD. |
