| First Author | Sternfeld M | Year | 2000 |
| Journal | Proc Natl Acad Sci U S A | Volume | 97 |
| Issue | 15 | Pages | 8647-52 |
| PubMed ID | 10890884 | Mgi Jnum | J:63406 |
| Mgi Id | MGI:1860977 | Doi | 10.1073/pnas.140004597 |
| Citation | Sternfeld M, et al. (2000) Excess 'read-through' acetylcholinesterase attenuates but the 'synaptic' variant intensifies neurodeterioration correlates. Proc Natl Acad Sci U S A 97(15):8647-52 |
| abstractText | Acute stress increases the risk for neurodegeneration, but the molecular signals regulating the shift from transient stress responses to progressive disease are not yet known. The 'read-through' variant of acetylcholinesterase (AChE-R) accumulates in the mammalian brain under acute stress. Therefore, markers of neurodeterioration were examined in transgenic mice overexpressing either AChE-R or the 'synaptic' AChE variant, AChE-S. Several observations demonstrate that excess AChE-R attenuates, whereas AChE-S intensifies, neurodeterioration. In the somatosensory cortex, AChE-S transgenics, but not AChE-R or control FVB/N mice, displayed a high density of curled neuronal processes indicative of hyperexcitation. In the hippocampus, AChE-S and control mice, but not AChE-R transgenics, presented progressive accumulation of clustered, heat shock protein 70-immunopositive neuronal fragments and displayed a high incidence of reactive astrocytes. Our findings suggest that AChE-R serves as a modulator that may play a role in preventing the shift from transient, acute stress to progressive neurological disease. |
