The effects of Rho GTPases’s modulation on CD1 outbred mice. Evaluation of behavior and brain metabolism of two different pharmacological approaches. The Rho GTPases are key regulators of actin cytoskeleton that modulate neuronal plasticity and have been linked to age-related cognitive diseases such as Alzheimer’s disease. In this preclinical study, we treated CD1 male mice with two different molecules studied for AD treatment: CNF1, a toxin which permanently activates the RhoGTPases, and fasudil, an inhibitor of the RhoGTPases downstream effector ROCKs. Our aim is to evaluate the pharmacological effects on the CNS of the two treatments using natural outbred murine models.
The effects of Rho GTPases’s modulation on CD1 outbred mice; evaluation of behavior and brain metabolism of two different pharmacological approaches / Dipol, Teresa; Zecca, Valentina; Palombelli, Gianmauro; Fortuna, Andrea; Morsilli, Ornella; Ricceri, Laura; Canese, Rossella; Loizzo, Stefano. - (2023). (Intervento presentato al convegno NeuroMi23 Meeting of the Milan Center for Neuroscience tenutosi a Milano).
The effects of Rho GTPases’s modulation on CD1 outbred mice; evaluation of behavior and brain metabolism of two different pharmacological approaches
Dipol Teresa;Zecca Valentina;
2023
Abstract
The effects of Rho GTPases’s modulation on CD1 outbred mice. Evaluation of behavior and brain metabolism of two different pharmacological approaches. The Rho GTPases are key regulators of actin cytoskeleton that modulate neuronal plasticity and have been linked to age-related cognitive diseases such as Alzheimer’s disease. In this preclinical study, we treated CD1 male mice with two different molecules studied for AD treatment: CNF1, a toxin which permanently activates the RhoGTPases, and fasudil, an inhibitor of the RhoGTPases downstream effector ROCKs. Our aim is to evaluate the pharmacological effects on the CNS of the two treatments using natural outbred murine models.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
