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How does CLN3 deficiency lead to neuronal cell death in Batten disease?
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Lysosome Function in Brain Health and Disease - From Tool Development to Novel Biology
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- 1 Intro
- 2 The lysosome is an example of the optimized subcellular biochemistry: it degrades macromolecules to recycle their nutrient content
- 3 Understanding these functions might be key for understanding a wide range of human disease
- 4 Subcellular metabolism as a new approach to study organelle dysfunction in human disease
- 5 Untargeted metabolomics reveals the accumulation of Glycerophosphodiesters (GPDs) in CLN3 deficient lysosomes
- 6 How does CLN3 deficiency lead to neuronal cell death in Batten disease?
- 7 Decreased contribution of GPC-derived choline to lipid biosynthesis in CLN3 KO-neurons
- 8 Lysosomal choline metabolism is essential for brain homeostasis
- 9 Choline: an essential metabolite in physiology
- 10 What are the principal sources of choline?
- 11 Endolysosomal CRISPR-Cas9 screen to identify lysosomal proteins important for surviving choline deprivation
- 12 Phosphocholine and choline are not accumulating in SPNS1- deficient lysosomes
- 13 SPNS1-deficient lysosomes accumulate lysophosphocholine (LPC) and lysophosphoethanolamine (LPE)
- 14 LPCs generated in lysosomes are trapped in SPNS1-deficient lysosomes
- 15 SPNS1 is a lysosomal lysophospholipid transporter
- 16 A novel lysosomal phospholipid salvage pathway
