Velázquez-Palacio R, Rodríguez-Labrada R, Velázquez-Pérez L

Language: Spanish
References: 0
Page: 55-65
PDF size: 157.42 Kb.

ABSTRACT

The effect of zinc deficiency in the development and function of the cerebellum has been studied in animal models and human beings. In the central nervous system, it exerts a modulatory function on synaptic transmission of the brain cortex, hippocampus and cerebellum. Zinc dishomeostasia is related with differents neurodegenerative diseases such as Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis and spinocerebellar ataxia type 2 (SCA2). It has shown a significant association between zinc levels and CAG expansion, suggesting new evidences on the role of zinc in the pathophysiological mechanisms of neurodegenerative diseases. The performance of a randomized, double-blind, placebo-controlled clinical trial in SCA2 patients demonstrated the efficacy and safety of Zn supplementation. The increase of zinc levels was associated with improvement of cerebellar syndrome, cognitive abnormalities, the decrease of lipid peroxidation and the reduction of saccadic latency, indicating the efficacy of the zinc supplementation for the symptomatic treatment of SCA2. This findings identifies the SCA2 disease as a valuable model for understanding the functions of zinc in the CNS, focus in the cerebellum. Besides, it indicates the need to extend these studies to other forms of Spinocerebellar Ataxias and neurodegenerative diseases which share the same pathophysiological mechanism.