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Neuronal ceroid-lipofuscinoses (NCL) are a group of inherited lysosomal storage disorders, characterized by accumulation of autofluorescent storage material. In NCLs, the hexosaminidase A enzyme activity is decreased in childhood, with subsequently severe neurological clinical manifestations, including psychomotor retardation and epilepsy. The aim of this study was to investigate whether the impairment of the guanidinoacetate methyltransferase (GAMT) activity, which is increased in NCLs, is associated with a higher degree of neurodegeneration and the appearance of epilepsy in NCL mice. GAMT enzymatic activity was decreased by 76.5 +/- 7.6% in a mouse model of juvenile neuronal ceroid-lipofuscinoses and by 64.0 +/- 8.4% in a mouse model of late-infantile NCL compared with controls. GAMT expression is increased by approximately 25-fold in the neural tissue of GAMT knockout (KO) mice; however, no significant changes in storage material accumulation and lysosomal membrane enzyme activities were observed in the GAMT KO mice. The results suggest that the inhibition of GAMT may contribute to the clinical manifestation of epilepsy and neuronal degeneration in NCLs..
**Authorship Contributions**
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https://colab.research.google.com/drive/1NOkYmenUX5kNPYWaFigLr_KvTvSHSIe1
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