Abstract
Batten disease is a group of fatal genetic diseases that are the leading cause of neurodegeneration in children. This study focused on six forms of Batten disease, each caused by the mutation of a ceroid lipofuscinosis, neuronal (CLN) gene - which encode proteins involved in lysosome function. Mutations are expected to alter neuronal lysosome function and potentially global neuronal morphology. Accumulation of the protein alpha-synuclein, a hallmark of Parkinson's disease, is a neuronal phenotype identified in some forms of Batten disease. This study aimed to investigate the pathologies in human neuronal models of CLN2, 3, 5, 6, 10, and 12 Batten disease.