FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4385651608> ?p ?o ?g. }

• W4385651608 abstract "Abstract Background Sarcopenia, an age‐related loss of muscle mass, is a critical factor that affects the health of the older adults. The SOD1KO mouse is deficient of Cu/Zn superoxide dismutase, used as an accelerated aging model. We previously showed that NT‐3 improves muscle fibre size by activating the mTOR pathway, suggesting a potential for attenuating age‐related muscle loss. This study assessed the therapeutic efficacy of AAV1.NT‐3 in this accelerated aging model. Methods Twelve 6 months old SOD1KO mice were injected intramuscularly with a 1 × 10 11 vg dose of AAV1.tMCK.NT‐3, and 13 age‐matched SOD1KO mice were used as controls. The treatment effect was evaluated using treadmill, rotarod and gait analyses as well as histological studies assessing changes in muscle fibre, and fibre type switch, in tibialis anterior, gastrocnemius, and triceps muscles, and myelin thickness by calculating G ratio in sciatic and tibial nerves. Molecular studies involved qPCR experiments to analyse the expression levels of mitochondrial and glycolysis markers and western blot experiments to assess the activity of mTORC1 pathway. Results Treatment resulted in a 36% (154.9 vs. 114.1; P < 0.0001) and 76% increase (154.3 vs. 87.6; P < 0.0001) in meters ran, with treadmill test at 3 and 6 months post gene delivery. In addition, the treated cohort stayed on rotarod 30% (52.7 s vs. 40.4 s; P = 0.0095) and 54% (50.4 s vs. 32.7 s; P = 0.0007) longer, compared with untreated counterparts at 3 and 6 months post injection. Gait analysis, performed at endpoint, showed that stride width was normalized to wild type levels (29.3 mm) by an 11% decrease, compared with untreated cohort (28.6 mm vs. 32.1 mm; P = 0.0014). Compared with wild‐type, SOD1KO mice showed 9.4% and 11.4% fibre size decrease in tibialis anterior and gastrocnemius muscles, respectively, which were normalized to wild type levels with treatment. Fibre diameter increase was observed prominently in FTG fibre type. G ratio analysis revealed hypomyelination in the tibial (0.721) and sciatic (0.676) nerves of SOD1KO model, which was reversed in the NT‐3 cohort (0.646 and 0.634, respectively). Fibre size increase correlated with the increase in the p‐S6 and p‐4E‐BP1 levels, and in the glycolysis markers in tibialis anterior. Alterations observed in the mitochondrial markers were not rescued with treatment. Overall, response to NT‐3 was subdued in gastrocnemius muscle. Conclusions This study shows that AAV1.NT‐3 gene therapy protected SOD1KO mouse from accelerated aging effects functionally and histologically. We further confirmed that NT‐3 has potential to activate the mTOR and glycolytic pathways in muscle." @default.
• W4385651608 created "2023-08-09" @default.
• W4385651608 creator A5003380664 @default.
• W4385651608 creator A5016629548 @default.
• W4385651608 creator A5037209981 @default.
• W4385651608 creator A5039394872 @default.
• W4385651608 creator A5043500922 @default.
• W4385651608 creator A5048041840 @default.
• W4385651608 date "2023-08-08" @default.
• W4385651608 modified "2023-10-16" @default.
• W4385651608 title "AAV1.NT‐3 gene therapy in the SOD1KO mouse model of accelerated sarcopenia" @default.
• W4385651608 cites W176186787 @default.
• W4385651608 cites W1964166589 @default.
• W4385651608 cites W1965011525 @default.
• W4385651608 cites W1974434128 @default.
• W4385651608 cites W1992631886 @default.
• W4385651608 cites W2004643937 @default.
• W4385651608 cites W2039663806 @default.
• W4385651608 cites W2040751146 @default.
• W4385651608 cites W2045291659 @default.
• W4385651608 cites W2047232246 @default.
• W4385651608 cites W2056791346 @default.
• W4385651608 cites W2062060047 @default.
• W4385651608 cites W2082564115 @default.
• W4385651608 cites W2083718982 @default.
• W4385651608 cites W2089835132 @default.
• W4385651608 cites W2101542622 @default.
• W4385651608 cites W2114760788 @default.
• W4385651608 cites W2127063807 @default.
• W4385651608 cites W2144365152 @default.
• W4385651608 cites W2149142681 @default.
• W4385651608 cites W2181268165 @default.
• W4385651608 cites W2242765960 @default.
• W4385651608 cites W2339005651 @default.
• W4385651608 cites W2606466125 @default.
• W4385651608 cites W2789744354 @default.
• W4385651608 cites W2810587571 @default.
• W4385651608 cites W2966183824 @default.
• W4385651608 cites W3035033574 @default.
• W4385651608 cites W3123116581 @default.
• W4385651608 cites W3126834739 @default.
• W4385651608 cites W3158552092 @default.
• W4385651608 cites W3176518538 @default.
• W4385651608 cites W3211169741 @default.
• W4385651608 cites W4200283054 @default.
• W4385651608 cites W4200379278 @default.
• W4385651608 doi "https://doi.org/10.1002/jcsm.13303" @default.
• W4385651608 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37553101" @default.
• W4385651608 hasPublicationYear "2023" @default.
• W4385651608 type Work @default.
• W4385651608 citedByCount "0" @default.
• W4385651608 crossrefType "journal-article" @default.
• W4385651608 hasAuthorship W4385651608A5003380664 @default.
• W4385651608 hasAuthorship W4385651608A5016629548 @default.
• W4385651608 hasAuthorship W4385651608A5037209981 @default.
• W4385651608 hasAuthorship W4385651608A5039394872 @default.
• W4385651608 hasAuthorship W4385651608A5043500922 @default.
• W4385651608 hasAuthorship W4385651608A5048041840 @default.
• W4385651608 hasBestOaLocation W43856516081 @default.
• W4385651608 hasConcept C104317684 @default.
• W4385651608 hasConcept C126322002 @default.
• W4385651608 hasConcept C134018914 @default.
• W4385651608 hasConcept C185592680 @default.
• W4385651608 hasConcept C2776214593 @default.
• W4385651608 hasConcept C2776263037 @default.
• W4385651608 hasConcept C2776379899 @default.
• W4385651608 hasConcept C2776415932 @default.
• W4385651608 hasConcept C2779959927 @default.
• W4385651608 hasConcept C2781149210 @default.
• W4385651608 hasConcept C2781172350 @default.
• W4385651608 hasConcept C2781464450 @default.
• W4385651608 hasConcept C55493867 @default.
• W4385651608 hasConcept C71924100 @default.
• W4385651608 hasConceptScore W4385651608C104317684 @default.
• W4385651608 hasConceptScore W4385651608C126322002 @default.
• W4385651608 hasConceptScore W4385651608C134018914 @default.
• W4385651608 hasConceptScore W4385651608C185592680 @default.
• W4385651608 hasConceptScore W4385651608C2776214593 @default.
• W4385651608 hasConceptScore W4385651608C2776263037 @default.
• W4385651608 hasConceptScore W4385651608C2776379899 @default.
• W4385651608 hasConceptScore W4385651608C2776415932 @default.
• W4385651608 hasConceptScore W4385651608C2779959927 @default.
• W4385651608 hasConceptScore W4385651608C2781149210 @default.
• W4385651608 hasConceptScore W4385651608C2781172350 @default.
• W4385651608 hasConceptScore W4385651608C2781464450 @default.
• W4385651608 hasConceptScore W4385651608C55493867 @default.
• W4385651608 hasConceptScore W4385651608C71924100 @default.
• W4385651608 hasFunder F4320315434 @default.
• W4385651608 hasLocation W43856516081 @default.
• W4385651608 hasLocation W43856516082 @default.
• W4385651608 hasOpenAccess W4385651608 @default.
• W4385651608 hasPrimaryLocation W43856516081 @default.
• W4385651608 hasRelatedWork W1994263459 @default.
• W4385651608 hasRelatedWork W2022634924 @default.
• W4385651608 hasRelatedWork W2159802435 @default.
• W4385651608 hasRelatedWork W2463478234 @default.
• W4385651608 hasRelatedWork W3135654060 @default.
• W4385651608 hasRelatedWork W3210939416 @default.
• W4385651608 hasRelatedWork W4283359913 @default.
• W4385651608 hasRelatedWork W4287837702 @default.

• next