A review of the tools for creating animal models of Alzheimer’s Disease
“192 IgG-saporin binds selectively and irreversibly to low-affinity nerve growth factor receptor interrupting cholinergic neuronal protein synthesis.”
“Anti-DBH-SAP allows a selective and gradual lesioning of noradrenergic neurones in the brain stem nucleus locus coeruleus, the primary site of noradrenaline production in the CNS.”
Verkhratsky A, Parpura V, Rodriguez-Arellano J, & Zorec R. (2019). Astroglia in Alzheimer’s Disease. In A Verkhratsky, M Ho, R Zorec & V Parpura (Eds.), Neuroglia in Neurodegenerative Diseases (Vol. Advances in Experimental Medicine and Biology, vol 1175, pp. 273-324). Singapore: Springer.
Summary: 192-IgG-SAP binds selectively and irreversibly to low-affinity nerve growth factor receptor interrupting cholinergic neuronal protein synthesis was employed. Anti-DBH-SAP binds dopamine-β-hydroxylase, which is not only localized mainly in the cytosol, but also at the plasma membrane surface of noradrenergic neurons. Anti-DBH-SAP produced specific and dose-dependent depletions of locus coeruleus neurons, with no effects on other cholinergic, dopaminergic or serotonergic neuronal populations. The possibility to induce a partial or total noradrenergic loss (by varying the injected dose) makes this immunotoxic approach an ideal model to study events within the noradrenergic projection system, as they occur during age-related demise of locus coeruleus in humans.