Luke J. Haslett

TL;DR: The results indicate that vATPase deficiency in PS1 loss-of-function states causes lysosomal/autophagy deficits and contributes to abnormal cellular Ca(2+) homeostasis, thus linking two AD-related pathogenic processes through a common molecular mechanism.

TL;DR: A strong understanding of where the authors are in experimental understanding of the CLN3 gene, its regulation, gene product, protein structure, tissue distribution, biomarker use, and pathological responses to its deficiency lays the groundwork for determining therapeutic action plans.

TL;DR: It is suggested that both Ppt1−/− microglia and astrocytes are dysfunctional and may contribute to the neurodegeneration observed in CLN1 disease, suggesting that the pathogenic role of glia may differ between NCLs.

TL;DR: The lysosome is of fundamental importance in the pathophysiology of diseases of ageing and by comparing against the LSDs the authors not only identify common pathways but also therapeutic targets so that ultimately more effective treatments can be developed for all neurodegenerative diseases.

TL;DR: The findings suggest that care should be taken when contemplating the use of curcumin supplements for NPC disease, and some caused elevations in NPC lysosomal storage and/or decreased cellular viability.