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Retinal neurodegeneration in different risk phenotypes of diabetic retinal disease

2021-12-21Journal article Open access
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dc.contributor.authorMadeira, Maria H.
dc.contributor.authorMarques, Inês P.
dc.contributor.authorFerreira, Sónia
dc.contributor.authorTavares, Diana
dc.contributor.authorSantos, Torcato
dc.contributor.authorSantos, Ana Rita
dc.contributor.authorFigueira, João
dc.contributor.authorLobo, Conceição
dc.contributor.authorCunha-Vaz, José
dc.date.accessioned2022-04-28T13:24:36Z
dc.date.available2022-04-28T13:24:36Z
dc.date.issued2021-12-21
dc.description.abstractDiabetic retinopathy (DR) has been considered a microvascular disease, but it has become evident that neurodegeneration also plays a key role in this complex pathology. Indeed, this complexity is reflected in its progression which occurs at different rates in different type 2 diabetic (T2D) individuals. Based on this concept, our group has identified three DR progression phenotypes that might reflect the interindividual differences: phenotype A, characterized by low microaneurysm turnover (MAT <6), phenotype B, low MAT (<6) and increased central retinal thickness (CRT); and phenotype C, with high MAT (≥6). In this study, we evaluated the progression of DR neurodegeneration, considering ganglion cell+inner plexiform layers (GCL+IPL) thinning, in 170 T2D individuals followed for a period of 5 years, to explore associations with disease progression or risk phenotypes. Ophthalmological examinations were performed at baseline, first 6 months, and annually. GCL+IPL average thickness was evaluated by optical coherence tomography (OCT). Microaneurysm turnover (MAT) was evaluated using the RetMarkerDR. ETDRS level and severity progression were assessed in seven-field color fundus photography. In the overall population there was a significant loss in GCL+IPL (−0.147 μm/year), independently of glycated hemoglobin, age, sex, and duration of diabetes. Interestingly, this progressive thinning in GCL + IPL reached higher values in phenotypes B and C (−0.249 and −0.238 μm/year, respectively), whereas phenotype A remained relatively stable. The presence of neurodegeneration in all phenotypes suggests that it is the retinal vascular response to the early neurodegenerative changes that determines the course of the retinopathy in each individual. Therefore, classification of different DR phenotypes appears to offer relevant clarification of DR disease progression and an opportunity for improved management of each T2D individual with DR, thus playing a valuable role for the implementation of personalized medicine in DR.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMadeira, M. H., Marques, I. P., Ferreira, S., Tavares, D., Santos, T., Santos, A. R., Figueira, J., Lobo, C., & Cunha-Vaz, J. (2021). Retinal Neurodegeneration in Different Risk Phenotypes of Diabetic Retinal Disease [Original Research]. Frontiers in Neuroscience, 15. https://doi.org/10.3389/fnins.2021.800004pt_PT
dc.identifier.doi10.3389/fnins.2021.800004pt_PT
dc.identifier.eissn1662-453X
dc.identifier.issn1662-4548
dc.identifier.urihttp://hdl.handle.net/10400.22/20423
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherFrontierspt_PT
dc.relation.ispartofseriesArtigo;800004
dc.relation.publisherversionhttps://www.frontiersin.org/articles/10.3389/fnins.2021.800004/fullpt_PT
dc.subjectDiabetespt_PT
dc.subjectRetinopathypt_PT
dc.subjectNeurodegenerationpt_PT
dc.subjectProgressionpt_PT
dc.subjectPersonalized medicinept_PT
dc.subjectRisk phenotypespt_PT
dc.titleRetinal neurodegeneration in different risk phenotypes of diabetic retinal diseasept_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage9pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleFrontiers in Neurosciencept_PT
oaire.citation.volume15pt_PT
person.familyNameB M Santos
person.givenNameAna Rita
person.identifier.ciencia-id291A-15C5-9C96
person.identifier.orcid0000-0003-3761-3292
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationcf304315-48a2-4bae-a1d5-61a4c8e45274
relation.isAuthorOfPublication.latestForDiscoverycf304315-48a2-4bae-a1d5-61a4c8e45274

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