{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T05:07:53Z","timestamp":1789708073532,"version":"4.0.1"},"reference-count":55,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T00:00:00Z","timestamp":1789689600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Mol. Biosci."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>X-linked adrenoleukodystrophy (X-ALD) has highly variable phenotypes with no known genotype\/phenotype correlation or method for predicting the course of the disease. Screening for X-ALD allows for early, potentially lifesaving treatment of adrenal insufficiency and cerebral demyelination, possibly useful to detect pre-clinical differences in patients and extend treatments to pre-symptomatic subjects. In this study, we analyzed the lipid signature in fibroblasts of patients with Adrenomyeloneuropathy (AMN), the late onset and slowly progressive form of X-ALD, and in patients with Cerebral Adrenoleukodystrophy (CALD), the cerebral inflammatory demyelinating form of early childhood, in order to identify specific lipid molecules as potential early predictors for CALD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We analyzed lipidomic profiles in fibroblasts obtained from n = 4 clinically affected (and genetically proven) X-ALD patients (two CALD and two AMN) and n = 4 age-matched controls, using a Dionex UltiMate 3000 UHPLC system, coupled to a Q-Exactive mass spectrometer.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Our results highlight alterations in lipid metabolism both in AMN and in CALD fibroblasts relative to controls, further confirming the role of LPC 26:0 as a potential biomarker of X-ALD. However, the extent and pattern of lipid remodeling differ substantially between the two phenotypes, with a contribution of neutral lipids in CALD patients, along with a selective involvement of gangliosides.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Although both AMN and CALD fibroblasts share some disease-associated lipid alterations, CALD samples exhibited a broader and more pronounced perturbation in multiple lipid classes, particularly in LPCs and steryl esters. The identification of phenotype-associated lipid signatures may represent a step forward toward precision medicine in X-ALD, in order to improve patient phenotypic evaluation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fmolb.2026.1906499","type":"journal-article","created":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T04:32:39Z","timestamp":1789705959000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Lipid signature in X-ALD: a comparison between phenotypes"],"prefix":"10.3389","volume":"13","author":[{"given":"Alessandra","family":"Di Veroli","sequence":"first","affiliation":[{"name":"Department of Chemistry, Biology and Biotechnology, University of Perugia - C.U.R.I. 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