000151053 001__ 151053
000151053 005__ 20251017144633.0
000151053 0247_ $$2doi$$a10.3390/genes13050865
000151053 0248_ $$2sideral$$a129148
000151053 037__ $$aART-2022-129148
000151053 041__ $$aeng
000151053 100__ $$0(orcid)0000-0001-5193-7782$$aCalvo, Ana Cristina$$uUniversidad de Zaragoza
000151053 245__ $$aLessons to Learn from the Gut Microbiota: A Focus on Amyotrophic Lateral Sclerosis
000151053 260__ $$c2022
000151053 5060_ $$aAccess copy available to the general public$$fUnrestricted
000151053 5203_ $$aThe gut microbiota is able to modulate the development and homeostasis of the central nervous system (CNS) through the immune, circulatory, and neuronal systems. In turn, the CNS influences the gut microbiota through stress responses and at the level of the endocrine system. This bidirectional communication forms the “gut microbiota–brain axis” and has been postulated to play a role in the etiopathology of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Numerous studies in animal models of ALS and in patients have highlighted the close communication between the immune system and the gut microbiota and, therefore, it is possible that alterations in the gut microbiota may have a direct impact on neuronal function and survival in ALS patients. Consequently, if the gut dysbiosis does indeed play a role in ALS-related neurodegeneration, nutritional immunomodulatory interventions based on probiotics, prebiotics, and/or postbiotics could emerge as innovative therapeutic strategies. This review aimed to shed light on the impact of the gut microbiota in ALS disease and on the use of potential nutritional interventions based on different types of biotics to ameliorate ALS symptoms.
000151053 536__ $$9info:eu-repo/grantAgreement/ES/ISCIII/FEDER/PI21-00372
000151053 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttps://creativecommons.org/licenses/by/4.0/deed.es
000151053 590__ $$a3.5$$b2022
000151053 591__ $$aGENETICS & HEREDITY$$b66 / 171 = 0.386$$c2022$$dQ2$$eT2
000151053 592__ $$a0.924$$b2022
000151053 593__ $$aGenetics (clinical)$$c2022$$dQ2
000151053 593__ $$aGenetics$$c2022$$dQ2
000151053 594__ $$a5.1$$b2022
000151053 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000151053 700__ $$aValledor-Martín, Inés
000151053 700__ $$0(orcid)0000-0002-7277-4318$$aMoreno-Martínez, Laura$$uUniversidad de Zaragoza
000151053 700__ $$0(orcid)0000-0002-7243-1737$$aToivonen, Janne Markus$$uUniversidad de Zaragoza
000151053 700__ $$0(orcid)0000-0001-5687-6704$$aOsta, Rosario$$uUniversidad de Zaragoza
000151053 7102_ $$11001$$2420$$aUniversidad de Zaragoza$$bDpto. Anatom.,Embri.Genét.Ani.$$cÁrea Genética
000151053 7102_ $$11012$$2315$$aUniversidad de Zaragoza$$bDpto. Farmac.Fisiol.y Med.L.F.$$cÁrea Farmacología
000151053 773__ $$g13, 5 (2022), 865 [13 pp.]$$pGenes (Basel)$$tGenes$$x2073-4425
000151053 8564_ $$s308784$$uhttps://zaguan.unizar.es/record/151053/files/texto_completo.pdf$$yVersión publicada
000151053 8564_ $$s2636624$$uhttps://zaguan.unizar.es/record/151053/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000151053 909CO $$ooai:zaguan.unizar.es:151053$$particulos$$pdriver
000151053 951__ $$a2025-10-17-14:27:33
000151053 980__ $$aARTICLE