| First Author | Pacheco-Quinto J | Year | 2016 |
| Journal | Neurobiol Aging | Volume | 48 |
| Pages | 83-92 | PubMed ID | 27644077 |
| Mgi Jnum | J:239563 | Mgi Id | MGI:5829156 |
| Doi | 10.1016/j.neurobiolaging.2016.08.011 | Citation | Pacheco-Quinto J, et al. (2016) Major amyloid-beta-degrading enzymes, endothelin-converting enzyme-2 and neprilysin, are expressed by distinct populations of GABAergic interneurons in hippocampus and neocortex. Neurobiol Aging 48:83-92 |
| abstractText | Impaired clearance of amyloid-beta peptide (Abeta) has been postulated to significantly contribute to the amyloid accumulation typical of Alzheimer's disease. Among the enzymes known to degrade Abeta in vivo are endothelin-converting enzyme (ECE)-1, ECE-2, and neprilysin (NEP), and evidence suggests that they regulate independent pools of Abeta that may be functionally significant. To better understand the differential regulation of Abeta concentration by its physiological degrading enzymes, we characterized the cell and region-specific expression pattern of ECE-1, ECE-2, and NEP by in situ hybridization and immunohistochemistry in brain areas relevant to Alzheimer's disease. In contrast to the broader distribution of ECE-1, ECE-2 and NEP were found enriched in GABAergic neurons. ECE-2 was majorly expressed by somatostatin-expressing interneurons and was active in isolated synaptosomes. NEP messenger RNA was found mainly in parvalbumin-expressing interneurons, with NEP protein localized to perisomatic parvalbuminergic synapses. The identification of somatostatinergic and parvalbuminergic synapses as hubs for Abeta degradation is consistent with the possibility that Abeta may have a physiological function related to the regulation of inhibitory signaling. |
