The winner of the Szent-Györgyi Student of the Year Prize is from the Biological Research Centre


The Foundation for the Future of Biomedical Sciences in Szeged, the Biological Research Centre and the University of Szeged organized the 15th Meeting of Nobel Laureates and Talented Students. This year Valéria Meszlényi received the Szent-Györgyi Student of the Year Prize at the 2-days conference (3-4, December). Vali - with the mentoring of László Siklós - investigates an incurable neurodegenerative disease, called amyotrophic lateral sclerosis (ALS) in the Institute of Biophysics, BRC. In her presentation she summarized the latest results in the field, the abstract of which we publish without change (source:


Alterations of motor axon terminals in mice due to passive transfer with sera of amyotrophic lateral sclerosis patients with identified mutations

Introduction: Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease affecting the motor neurons in the brain and spinal cord, leading to the loss of voluntary muscle function. ALS can be classified as familial or sporadic based on its inheritance. Previously, our research group demonstrated an increase of the calcium level and increase of the number of synaptic vesicles in the motor axon terminals (MATs) of sporadic ALS patients. These alterations could be conferred to mice via passive transfer of the sera from these patients. In the present experiment we aimed to question the similar effect of the sera from another population of patients, which possess identified mutations.

Methods: Patients with 11 different ALS-related mutations participated in our study. Balb/c mice were injected intraperitoneally with sera of ALS patients or healthy individuals for two days. After the passive transfer, calcium histochemistry was performed and MATs in the interosseus muscles were investigated under electron microscope. Intracellular calcium content and synaptic vesicle number was quantified.

Results: Passive transfer resulted in significant increase of intracellular calcium levels and synaptic vesicle number in the MATs of mice due to the passive transfer of sera from ALS patients with identified mutations, similar to sera from sporadic ALS patients. In addition, ultrastructural signs of degeneration were also observed at the neuro-muscular synapses.

Discussion: Our findings support the unifying hypothesis, that the pathomechanism underlying the identical manifestation of the disease with or without identified mutations is based on a common final pathway, in which calcium increase plays a central role.


Congratulations to Vali for the Prize and best wishes for her scientific work!


The video of the presentation is available at this link:

The interview with Vali will be available on the website