SwePub
Sök i LIBRIS databas

  Utökad sökning

WFRF:(Shoaie Saeed)
 

Sökning: WFRF:(Shoaie Saeed) > Combined Metabolic ...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005823naa a2200517 4500
001oai:DiVA.org:kth-346370
003SwePub
008240514s2024 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-3463702 URI
0247 a https://doi.org/10.3390/biomedicines120409272 DOI
040 a (SwePub)kth
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Altay, Özlemu KTH,Systembiologi,Science for Life Laboratory, SciLifeLab4 aut0 (Swepub:kth)u1g32ner
2451 0a Combined Metabolic Activators with Different NAD+ Precursors Improve Metabolic Functions in the Animal Models of Neurodegenerative Diseases
264 1b MDPI AG,c 2024
338 a print2 rdacarrier
500 a QC 20240514
520 a 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.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
653 a Alzheimer’s disease
653 a animal models
653 a combined metabolic activators
653 a Parkinson’s disease
7001 a Yang, Hongu KTH,Systembiologi,Science for Life Laboratory, SciLifeLab4 aut0 (Swepub:kth)u150v7zg
7001 a Yildirim, Serkanu Department of Pathology, Faculty of Veterinary Medicine, Atatürk University, Erzurum 25240, Turkey;4 aut
7001 a Bayram, Cemilu Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Atatürk University, Erzurum 25240, Turkey;4 aut
7001 a Bolat, Ismailu Department of Pathology, Faculty of Veterinary Medicine, Atatürk University, Erzurum 25240, Turkey;4 aut
7001 a Oner, Senau Department of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, 25240, Turkey4 aut
7001 a Tozlu, Ozlem Ozdemiru Department of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, 25240, Turkey4 aut
7001 a Arslan, Mehmet Enesu Department of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, 25240, Turkey4 aut
7001 a Hacimuftuoglu, Ahmetu Department of Medical Pharmacology, Faculty of Medicine, Atatürk University, Erzurum 25240, Turkey;4 aut
7001 a Shoaie, Saeedu Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, London, SE1 9RT, UK4 aut
7001 a Zhang, Chengu KTH,Systembiologi,Science for Life Laboratory, SciLifeLab4 aut0 (Swepub:kth)u1ww5kvp
7001 a Borén, Janu Department of Molecular and Clinical Medicine, Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, 413 45, Sweden4 aut
7001 a Uhlén, Mathiasu KTH,Systembiologi,Science for Life Laboratory, SciLifeLab4 aut0 (Swepub:kth)u1dulvmw
7001 a Turkez, Hasanu Department of Medical Biology, Faculty of Medicine, Atatürk University, Erzurum 25240, Turkey;4 aut
7001 a Mardinoglu, Adilu KTH,Systembiologi,Science for Life Laboratory, SciLifeLab,Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, London, SE1 9RT, UK4 aut0 (Swepub:kth)u1t8kmr6
7102 a KTHb Systembiologi4 org
7730 t Biomedicinesd : MDPI AGg 12:4q 12:4x 2227-9059
8564 u https://doi.org/10.3390/biomedicines12040927y Fulltext
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-346370
8564 8u https://doi.org/10.3390/biomedicines12040927

Hitta via bibliotek

Till lärosätets databas

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy