{"id":36377,"date":"2025-07-17T12:30:07","date_gmt":"2025-07-17T12:30:07","guid":{"rendered":"https:\/\/www.etap-lab.com\/?p=15906"},"modified":"2026-04-15T22:43:33","modified_gmt":"2026-04-15T20:43:33","slug":"publication-on-ndds-cellular-models-scientific-reports-nature","status":"publish","type":"ressource","link":"https:\/\/www.etap-lab.com\/en\/ressource\/publication-on-ndds-cellular-models-scientific-reports-nature\/","title":{"rendered":"Publication on NDD&#8217;s cellular models &#8211; Scientific Reports (Nature)"},"content":{"rendered":"<p><!--ScriptorStartFragment--><\/p>\n<div class=\"scriptor-paragraph\">Consult the publication in which ETAP-LAB was mentioned and acknowledged for our in vitro hippocampal neuron model\u2014challenged with own-manufactured Tau oligomers: &#8220;A novel allosteric GCase modulator prevents Tau accumulation in GBA1WT and GBA1L444P\/L444P cellular models. Sci Rep 15, 17646 (2025).&#8221;<\/div>\n<div class=\"scriptor-paragraph\">Published 21 May 2025 &#8211; Ciccaldo, M., P\u00e9rez-Carmona, N., Piovesana, E. et al. https:\/\/www.nature.com\/articles\/s41598-025-02346-8<\/div>\n<div><\/div>\n<div><strong>Authors<\/strong>: Matteo Ciccaldo1, Nat\u00e0lia P\u00e9rez-Carmona2, Ester Piovesana1, Sara Cano-Crespo2, Ana Ruano2, Aida Delgado2, Ilaria Fregno3, Beatriz Calvo-Flores Guzm\u00e1n4, Manolo Bellotto4, Maurizio Molinari3,5, Joanne Taylor6, St\u00e9phanie Papin1, Ana Mar\u00eda Garc\u00eda-Collazo2 &amp; Paolo Paganetti1,7,<\/div>\n<div><\/div>\n<div><strong>Abstract: <\/strong><\/div>\n<div>A slow decline in the autophagy-lysosomal pathway is a hallmark of the normal aging brain. Yet, an acceleration of this cellular function may propel neurodegenerative events. In fact, mutations in genes associated with the autophagy-lysosomal pathway can lead to Parkinson\u2019s disease. Also, amyloidogenic protein deposition is observed in lysosomal storage disorders, which are caused by genetic mutations representing risk factors for Parkinson\u2019s disease. For example, Gaucher\u2019s disease\u00a0<i>GBA1<\/i>\u00a0mutations leading to defects in lysosomal sphingolipid metabolism cause \u03b1-synuclein accumulation. We observed that increased lysosomal Tau accumulation is found in human dermal fibroblasts engineered for inducible Tau expression. Inhibition of the\u00a0<i>GBA1<\/i>\u00a0product GCase augmented Tau-dependent lysosomal stress and Tau accumulation. Here, we show increased Tau seed-induced Tau accumulation in Gaucher\u2019s fibroblasts carrying\u00a0<i>GBA1<\/i>\u00a0mutations when compared to normal fibroblasts. Pharmacological enhancement of GCase reversed this effect, notably, also in normal fibroblasts. This suggests that boosting GCase activity may represent a therapeutic strategy to slow down aging-dependent lysosomal deficits and brain protein deposition.<\/div>\n<p><!--ScriptorEndFragment--><\/p>\n<p>&nbsp;<\/p>\n<p><strong>Keywords<\/strong>: Alzheimer&#8217;s disease,\u00a0Mechanisms of disease, Parkinson&#8217;s disease<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Discover Publication on NDD&#8217;s cellular models &#8211; Scientific Reports (Nature): Consult the publication in which ETAP-LAB was mentioned and acknowledged for our in vitro hippocampal neuron\u2026<\/p>\n","protected":false},"featured_media":15911,"template":"","meta":{"_acf_changed":false},"categorie-de-ressource":[235],"marque-de-ressource":[],"class_list":["post-36377","ressource","type-ressource","status-publish","has-post-thumbnail","hentry","categorie-de-ressource-publications"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.5 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Publication on NDD&#039;s cellular models - 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