{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Martinez-Aleson P"],"funding":["Junta de Comunidades de Castilla-la Mancha","University San Pablo CEU-Santander precompetitive grants","Consejería de Educación, Ciencia y Universidades Comunidad de Madrid"],"pagination":["e70044"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12851830"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["46(1)"],"pubmed_abstract":["Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease (MND) characterized by progressive degeneration of both upper and lower motor neurons, along with skeletal muscles innervated by them. The identification of key molecules involved in disease pathology remains crucial for ALS, as no curative treatment is currently available. Pleiotrophin (PTN) and midkine (MK) are closely related, heparin-binding cytokines with overlapping effects. These molecules have been shown to be neuroprotective by modulating neuroinflammation, supporting neuronal survival, growth, and differentiation, and enhancing synaptic strength and plasticity. Despite their reported neuroprotective properties, the involvement of PTN and MK signaling in ALS has not been previously investigated. In this study, we "],"journal":["Neuropathology : official journal of the Japanese Society of Neuropathology"],"pubmed_title":["Pleiotrophin/Midkine Pathway Is Dysregulated in a TDP-43<sup>A315T</sup> Mouse Model of Amyotrophic Lateral Sclerosis (ALS)."],"pmcid":["PMC12851830"],"funding_grant_id":["FUSPBS-PPC03/2018","PIPF-2023/SAL-GL-29613","SBPLY/17/180501/000303"],"pubmed_authors":["Martinez-Aleson P","Benito-Casado C","Fernandez-Martos CM","Polanco Mora MJ"],"additional_accession":[]},"is_claimable":false,"name":"Pleiotrophin/Midkine Pathway Is Dysregulated in a TDP-43<sup>A315T</sup> Mouse Model of Amyotrophic Lateral Sclerosis (ALS).","description":"Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease (MND) characterized by progressive degeneration of both upper and lower motor neurons, along with skeletal muscles innervated by them. The identification of key molecules involved in disease pathology remains crucial for ALS, as no curative treatment is currently available. Pleiotrophin (PTN) and midkine (MK) are closely related, heparin-binding cytokines with overlapping effects. These molecules have been shown to be neuroprotective by modulating neuroinflammation, supporting neuronal survival, growth, and differentiation, and enhancing synaptic strength and plasticity. Despite their reported neuroprotective properties, the involvement of PTN and MK signaling in ALS has not been previously investigated. In this study, we ","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-06-13T03:13:03.647Z","creation":"2026-06-13T03:08:51.582Z"},"accession":"S-EPMC12851830","cross_references":{"pubmed":["41605460"],"doi":["10.1111/neup.70044"]}}