| First Author | Epelbaum S | Year | 2015 |
| Journal | Neurobiol Aging | Volume | 36 |
| Issue | 6 | Pages | 2043-52 |
| PubMed ID | 25862419 | Mgi Jnum | J:318266 |
| Mgi Id | MGI:6858988 | Doi | 10.1016/j.neurobiolaging.2015.03.005 |
| Citation | Epelbaum S, et al. (2015) Acute amnestic encephalopathy in amyloid-beta oligomer-injected mice is due to their widespread diffusion in vivo. Neurobiol Aging 36(6):2043-52 |
| abstractText | Amyloid-beta (Abeta) oligomers are the suspected culprit as initiators of Alzheimer's disease (AD). However, their diffusion in the brain remains unknown. Here, we studied Abeta oligomers' dissemination and evaluated their in vivo toxicity. Wild-type mice were injected with 50 pmol of synthetic Abeta oligomers (of different size) in the hippocampus. Oligomers diffused largely in the brain as soon as 1 hour and up to 7 days after injection. A transient encephalopathy with memory impairment was induced by this unique injection. The immunoreactivity of the postsynaptic marker PSD95 was diffusely decreased. Similar results (both on memory and PSD95 immunoreactivity) were obtained with delipidated and high molecular weight oligomers (>50 kDa) but not with smaller assemblies. Tau hyperphosphorylation was observed in the oligomer-injected brains. Finally, fos immunostaining was increased in Abeta-derived diffusible ligands-injected mice, suggesting neuronal hyperactivity. Rapid and widespread diffusion of Abeta oligomers was demonstrated in vivo and associated with decreased synaptic markers and memory deficits which gives new insight to the pathogenicity of Abeta. |
