Abstract
Abstract CLN3 is a lysosomal transmembrane protein and loss of CLN3 mutation is known to cause a juvenile lethal neurodegenerative lysosomal storage disorder (LSD), called Batten disease. In a recent study published in Nature, Laqtom et al. reported a novel function of CLN3 in the clearance of glycerophospholipid from lysosomes via lysosomal efflux of glycerophosphodiesters (GPDs), not only establishing a deeper mechanistic understanding of Batten disease, also suggesting both the diagnostic and therapeutic potential of CLN3-GPDs in this type of neurodegenerative LSD.
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