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Arun Mahato

University of Helsinki, Finland

Title: Small molecule GDNF receptor RET agonist supports the survival of dopamine neurons in vitro and protects their function in 6-OHDA lesioned rat midbrain

Biography

Biography: Arun Mahato

Abstract

Motor symptoms of Parkinson’s disease (PD) are caused by degeneration and progressive loss of nigrostriatal dopamine
neurons and affect up to 6–7 million people world-wide. Currently no cure for this disease is available. Existing
therapeutic strategies based on dopamine replacement, alleviate PD symptoms, but do not prevent or slow down degeneration
of dopamine neurons. Glial cell line-derived neurotrophic factor (GDNF) and its closely related protein neurturin (NRTN)
can protect and repair dopamine neurons in vitro and in animal models of PD, but their clinical use is complicated because of
their low bioavailability and poor diffusion in tissues. Previously, we discovered a small molecule called BT13 that selectively
activates GDNF receptors and promotes neurite outgrowth from sensory neurons. Here, we report the ability of this molecule
to support the survival of cultured dopamine neurons only when they express GDNF receptors. In addition, BT13 activates
intracellular signaling cascades in vivo, stimulates release of dopamine and protect the function of dopaminergic neurons in
a 6-hydroxydopamine (6-OHDA) rat model of PD. In contrast to GDNF, BT13 is able to penetrate through the blood-brainbarrier
and it spreads well in brain tissue. Thus, although its solubility and stability require optimization, BT13 serves as an
excellent tool compound for the development of novel disease-modifying treatments against PD.