{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T15:24:54Z","timestamp":1791991494232,"version":"4.4.0"},"posted":{"date-parts":[[2026,3,21]]},"group-title":"Cell Biology","reference-count":103,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T00:00:00Z","timestamp":1774051200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100014989","name":"Chan Zuckerberg Initiative","doi-asserted-by":"crossref","award":["2024-338545"],"award-info":[{"award-number":["2024-338545"]}],"id":[{"id":"10.13039\/100014989","id-type":"DOI","asserted-by":"crossref"}]},{"name":"NCL Foundation"},{"name":"Knight Initiative for Brain Resilience at Stanford University"},{"id":[{"id":"https:\/\/ror.org\/00wra1b14","id-type":"ROR","asserted-by":"publisher"}]},{"name":"NIH Director\u2019s New Innovator Award Program","award":["1DP2CA271386"],"award-info":[{"award-number":["1DP2CA271386"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,3,21]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  CLN5 Batten disease, caused by biallelic mutations in\n                  <jats:italic>CLN5<\/jats:italic>\n                  , is a rare, early-onset neurodegenerative lysosomal storage disorder that has no cure and lacks validated biomarkers, hindering accurate diagnosis and assessment of therapeutic response. We recently identified CLN5 as the synthase of bis(monoacylglycero)phosphate (BMP), an endolysosomal phospholipid crucial for lysosome function and lipid catabolism. This suggested BMP and its precursor lysophosphatidylglycerol (LPG) as clinically relevant biomarkers. It also prompted\n                  <jats:italic>in vivo<\/jats:italic>\n                  confirmation of CLN5 as the biologically relevant lysosomal BMP synthase. Here we show that murine and ovine disease models lacking CLN5 show significant and universal depletion of BMP and elevation of LPG across tissues and brain regions, consistent with the biochemical function of CLN5. Additionally, lysosomal lysates from murine models of CLN5 Batten disease lack the ability to synthesize BMP from its precursor LPG, establishing CLN5 as the main BMP synthase\n                  <jats:italic>in vivo<\/jats:italic>\n                  . Of importance, CLN5 patient-derived fibroblasts show BMP depletion and LPG elevation. Translating these results towards clinical utility, we demonstrate BMP and LPG to be accessible biomarkers for CLN5 Batten disease in both plasma and dried blood spots, enabling early diagnosis and patient screening.\n                <\/jats:p>","DOI":"10.64898\/2026.03.19.712969","type":"posted-content","created":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T21:45:13Z","timestamp":1774129513000},"source":"Crossref","is-referenced-by-count":4,"title":["Translational lipidomics reveals BMP and its precursor LPG as biomarkers for CLN5 Batten disease"],"prefix":"10.64898","author":[{"given":"Eshaan S.","family":"Rawat","sequence":"first","affiliation":[{"name":"Department of Chemical Engineering, Stanford University, Stanford, CA, 94305, USA"},{"name":"Department of Genetics, Stanford University, Stanford, CA, 94305, USA"},{"name":"The Institute for Chemistry, Engineering & Medicine for Human Health (Sarafan ChEM-H), Stanford University, Stanford, CA, 94305, USA"},{"name":"Present 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