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  • Altay, ÖzlemKTH,Systembiologi,Science for Life Laboratory, SciLifeLab (författare)

Combined Metabolic Activators with Different NAD+ Precursors Improve Metabolic Functions in the Animal Models of Neurodegenerative Diseases

  • Artikel/kapitelEngelska2024

Förlag, utgivningsår, omfång ...

  • MDPI AG,2024
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:kth-346370
  • https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-346370URI
  • https://doi.org/10.3390/biomedicines12040927DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • QC 20240514
  • Background: Mitochondrial dysfunction and metabolic abnormalities are acknowledged as significant factors in the onset of neurodegenerative disorders such as Parkinson’s disease (PD) and Alzheimer’s disease (AD). Our research has demonstrated that the use of combined metabolic activators (CMA) may alleviate metabolic dysfunctions and stimulate mitochondrial metabolism. Therefore, the use of CMA could potentially be an effective therapeutic strategy to slow down or halt the progression of PD and AD. CMAs include substances such as the glutathione precursors (L-serine and N-acetyl cysteine), the NAD+ precursor (nicotinamide riboside), and L-carnitine tartrate. Methods: Here, we tested the effect of two different formulations, including CMA1 (nicotinamide riboside, L-serine, N-acetyl cysteine, L-carnitine tartrate), and CMA2 (nicotinamide, L-serine, N-acetyl cysteine, L-carnitine tartrate), as well as their individual components, on the animal models of AD and PD. We assessed the brain and liver tissues for pathological changes and immunohistochemical markers. Additionally, in the case of PD, we performed behavioral tests and measured responses to apomorphine-induced rotations. Findings: Histological analysis showed that the administration of both CMA1 and CMA2 formulations led to improvements in hyperemia, degeneration, and necrosis in neurons for both AD and PD models. Moreover, the administration of CMA2 showed a superior effect compared to CMA1. This was further corroborated by immunohistochemical data, which indicated a reduction in immunoreactivity in the neurons. Additionally, notable metabolic enhancements in liver tissues were observed using both formulations. In PD rat models, the administration of both formulations positively influenced the behavioral functions of the animals. Interpretation: Our findings suggest that the administration of both CMA1 and CMA2 markedly enhanced metabolic and behavioral outcomes, aligning with neuro-histological observations. These findings underscore the promise of CMA2 administration as an effective therapeutic strategy for enhancing metabolic parameters and cognitive function in AD and PD patients.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Yang, HongKTH,Systembiologi,Science for Life Laboratory, SciLifeLab(Swepub:kth)u150v7zg (författare)
  • Yildirim, SerkanDepartment of Pathology, Faculty of Veterinary Medicine, Atatürk University, Erzurum 25240, Turkey; (författare)
  • Bayram, CemilDepartment of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Atatürk University, Erzurum 25240, Turkey; (författare)
  • Bolat, IsmailDepartment of Pathology, Faculty of Veterinary Medicine, Atatürk University, Erzurum 25240, Turkey; (författare)
  • Oner, SenaDepartment of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, 25240, Turkey (författare)
  • Tozlu, Ozlem OzdemirDepartment of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, 25240, Turkey (författare)
  • Arslan, Mehmet EnesDepartment of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, 25240, Turkey (författare)
  • Hacimuftuoglu, AhmetDepartment of Medical Pharmacology, Faculty of Medicine, Atatürk University, Erzurum 25240, Turkey; (författare)
  • Shoaie, SaeedCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, London, SE1 9RT, UK (författare)
  • Zhang, ChengKTH,Systembiologi,Science for Life Laboratory, SciLifeLab(Swepub:kth)u1ww5kvp (författare)
  • Borén, JanDepartment of Molecular and Clinical Medicine, Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, 413 45, Sweden (författare)
  • Uhlén, MathiasKTH,Systembiologi,Science for Life Laboratory, SciLifeLab(Swepub:kth)u1dulvmw (författare)
  • Turkez, HasanDepartment of Medical Biology, Faculty of Medicine, Atatürk University, Erzurum 25240, Turkey; (författare)
  • Mardinoglu, AdilKTH,Systembiologi,Science for Life Laboratory, SciLifeLab,Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, London, SE1 9RT, UK(Swepub:kth)u1t8kmr6 (författare)
  • KTHSystembiologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Biomedicines: MDPI AG12:42227-9059

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