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dc.contributor.authorLima Filho, Ricardo André Santanapt_BR
dc.contributor.authorBenedet, Andréa L.pt_BR
dc.contributor.authorDe Bastiani, Marco Antôniopt_BR
dc.contributor.authorPovala, Guilhermept_BR
dc.contributor.authorFerreira, Danielle Cozachencopt_BR
dc.contributor.authorFerreira, Sérgio Teixeirapt_BR
dc.contributor.authorDe Felice, Fernanda Guarinopt_BR
dc.contributor.authorRosa Neto, Pedropt_BR
dc.contributor.authorZimmer, Eduardo Rigonpt_BR
dc.contributor.authorLourenço, Mychael Vinícius da Costapt_BR
dc.contributor.otherAlzheimer’s Disease Neuroimaging Initiativept_BR
dc.date.accessioned2023-09-23T03:38:54Zpt_BR
dc.date.issued2023pt_BR
dc.identifier.issn2632-1297pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/265162pt_BR
dc.description.abstractFibronectin type III domain–containing protein 5 (FNDC5) and its derived hormone, irisin, have been associated with metabolic control in humans, with described FNDC5 single nucleotide polymorphisms being linked to obesity and metabolic syndrome. Decreased brain FNDC5/irisin has been reported in subjects with dementia due to Alzheimer’s disease. Since impaired brain glucose metabolism develops in ageing and is prominent in Alzheimer’s disease, here, we examined associations of a single nucleotide polymorphism in the FNDC5 gene (rs1746661) with brain glucose metabolism and amyloid-β deposition in a cohort of 240 cognitively unimpaired and 485 cognitively impaired elderly individuals from the Alzheimer’s Disease Neuroimaging Initiative. In cognitively unimpaired elderly individuals harbouring the FNDC5 rs1746661(T) allele, we observed a regional reduction in low glucose metabolism in memory-linked brain regions and increased brain amyloid-β PET load. No differences in cognition or levels of cerebrospinal fluid amyloid-β42, phosphorylated tau and total tau were observed between FNDC5 rs1746661(T) allele carriers and non-carriers. Our results indicate that a genetic variant of FNDC5 is associated with low brain glucose metabolism in elderly individuals and suggest that FNDC5 may participate in the regulation of brain metabolism in brain regions vulnerable to Alzheimer’s disease pathophysiology. Understanding the associations between genetic variants in metabolism-linked genes and metabolic brain signatures may contribute to elucidating genetic modulators of brain metabolism in humans.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofBrain communications. Oxford. Vol. 5, no. 4 (Aug. 2023), fcad216, 10 p.pt_BR
dc.rightsOpen Accessen
dc.subjectDoenças neurodegenerativaspt_BR
dc.subjectAlzheimer’s diseaseen
dc.subjectDoença de Alzheimerpt_BR
dc.subjectFNDC5/irisinen
dc.subjectPET-FDGen
dc.subjectTranstornos do metabolismo de glucosept_BR
dc.subjectPolimorfismo de nucleotídeo únicopt_BR
dc.subjectGlucose metabolismen
dc.subjectSingle nucleotide polymorphismen
dc.titleAssociation of the fibronectin type III domain–containing protein 5 rs1746661 single nucleotide polymorphism with reduced brain glucose metabolism in elderly humanspt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001177151pt_BR
dc.type.originEstrangeiropt_BR


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