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Retinal ganglion cell dysfunction in preclinical Alzheimer’s disease: an electrophysiologic biomarker signature
The current study evaluated retinal function using electroretinography (ERG) in cognitively healthy (CH) participants with preclinical Alzheimer’s disease (AD), as classified by cerebral spinal fluid (CSF) Aβ(42)/Tau ratio. Individuals with normal retinal morphology ascertained by spectral-domain op...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7973731/ https://www.ncbi.nlm.nih.gov/pubmed/33737516 http://dx.doi.org/10.1038/s41598-021-85010-1 |
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author | Asanad, Samuel Felix, Christian M. Fantini, Michele Harrington, Michael G. Sadun, Alfredo A. Karanjia, Rustum |
author_facet | Asanad, Samuel Felix, Christian M. Fantini, Michele Harrington, Michael G. Sadun, Alfredo A. Karanjia, Rustum |
author_sort | Asanad, Samuel |
collection | PubMed |
description | The current study evaluated retinal function using electroretinography (ERG) in cognitively healthy (CH) participants with preclinical Alzheimer’s disease (AD), as classified by cerebral spinal fluid (CSF) Aβ(42)/Tau ratio. Individuals with normal retinal morphology ascertained by spectral-domain optical coherence tomography were enrolled. Full-field ERG, pattern PERG, and photopic negative response (PhNR) were performed in 29 adult participants (58 eyes). Amplitude and implicit times of the ERG wave components were analyzed. Preclinical AD participants showed marked retinal ganglion cell dysfunction relative to controls. The PhNR was significantly diminished in preclinical AD relative to controls. PhNR amplitude and N95 implicit time differentiated CH individuals with CSF biomarkers of AD pathology with 87% sensitivity and 82% specificity. These quantitative electrophysiologic findings expand our understanding of early retinal functional changes that precede cognitive decline in AD. Retinal ganglion cell dysfunction, as detected by ERG, may be a clinically useful, non-invasive in vivo biomarker for early disease detection, which is necessary for ultimately pursuing early intervention. |
format | Online Article Text |
id | pubmed-7973731 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-79737312021-03-19 Retinal ganglion cell dysfunction in preclinical Alzheimer’s disease: an electrophysiologic biomarker signature Asanad, Samuel Felix, Christian M. Fantini, Michele Harrington, Michael G. Sadun, Alfredo A. Karanjia, Rustum Sci Rep Article The current study evaluated retinal function using electroretinography (ERG) in cognitively healthy (CH) participants with preclinical Alzheimer’s disease (AD), as classified by cerebral spinal fluid (CSF) Aβ(42)/Tau ratio. Individuals with normal retinal morphology ascertained by spectral-domain optical coherence tomography were enrolled. Full-field ERG, pattern PERG, and photopic negative response (PhNR) were performed in 29 adult participants (58 eyes). Amplitude and implicit times of the ERG wave components were analyzed. Preclinical AD participants showed marked retinal ganglion cell dysfunction relative to controls. The PhNR was significantly diminished in preclinical AD relative to controls. PhNR amplitude and N95 implicit time differentiated CH individuals with CSF biomarkers of AD pathology with 87% sensitivity and 82% specificity. These quantitative electrophysiologic findings expand our understanding of early retinal functional changes that precede cognitive decline in AD. Retinal ganglion cell dysfunction, as detected by ERG, may be a clinically useful, non-invasive in vivo biomarker for early disease detection, which is necessary for ultimately pursuing early intervention. Nature Publishing Group UK 2021-03-18 /pmc/articles/PMC7973731/ /pubmed/33737516 http://dx.doi.org/10.1038/s41598-021-85010-1 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Asanad, Samuel Felix, Christian M. Fantini, Michele Harrington, Michael G. Sadun, Alfredo A. Karanjia, Rustum Retinal ganglion cell dysfunction in preclinical Alzheimer’s disease: an electrophysiologic biomarker signature |
title | Retinal ganglion cell dysfunction in preclinical Alzheimer’s disease: an electrophysiologic biomarker signature |
title_full | Retinal ganglion cell dysfunction in preclinical Alzheimer’s disease: an electrophysiologic biomarker signature |
title_fullStr | Retinal ganglion cell dysfunction in preclinical Alzheimer’s disease: an electrophysiologic biomarker signature |
title_full_unstemmed | Retinal ganglion cell dysfunction in preclinical Alzheimer’s disease: an electrophysiologic biomarker signature |
title_short | Retinal ganglion cell dysfunction in preclinical Alzheimer’s disease: an electrophysiologic biomarker signature |
title_sort | retinal ganglion cell dysfunction in preclinical alzheimer’s disease: an electrophysiologic biomarker signature |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7973731/ https://www.ncbi.nlm.nih.gov/pubmed/33737516 http://dx.doi.org/10.1038/s41598-021-85010-1 |
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