Retinal nerve fiber layer thickness predicts CSF amyloid/tau before cognitive decline.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2020
Historique:
received: 23 01 2020
accepted: 21 04 2020
entrez: 30 5 2020
pubmed: 30 5 2020
medline: 1 8 2020
Statut: epublish

Résumé

Alzheimer's disease (AD) pathology precedes symptoms and its detection can identify at-risk individuals who may benefit from early treatment. Since the retinal nerve fiber layer (RNFL) is depleted in established AD, we tested whether its thickness can predict whether cognitively healthy (CH) individuals have a normal or pathological cerebrospinal fluid (CSF) Aß42 (A) and tau (T) ratio. As part of an ongoing longitudinal study, we enrolled CH individuals, excluding those with cognitive impairment and significant ocular pathology. We classified the CH group into two sub-groups, normal (CH-NAT, n = 16) or pathological (CH-PAT, n = 27), using a logistic regression model from the CSF AT ratio that identified >85% of patients with a clinically probable AD diagnosis. Spectral-domain optical coherence tomography (OCT) was acquired for RNFL, ganglion cell-inner plexiform layer (GC-IPL), and macular thickness. Group differences were tested using mixed model repeated measures and a classification model derived using multiple logistic regression. Mean age (± standard deviation) in the CH-PAT group (n = 27; 75.2 ± 8.4 years) was similar (p = 0.50) to the CH-NAT group (n = 16; 74.1 ± 7.9 years). Mean RNFL (standard error) was thinner in the CH-PAT group by 9.8 (2.7) μm; p < 0.001. RNFL thickness classified CH-NAT vs. CH-PAT with 87% sensitivity and 56.3% specificity. Our retinal data predict which individuals have CSF biomarkers of AD pathology before cognitive deficits are detectable with 87% sensitivity. Such results from easy-to-acquire, objective and non-invasive measurements of the RNFL merit further study of OCT technology to monitor or screen for early AD pathology.

Sections du résumé

BACKGROUND
Alzheimer's disease (AD) pathology precedes symptoms and its detection can identify at-risk individuals who may benefit from early treatment. Since the retinal nerve fiber layer (RNFL) is depleted in established AD, we tested whether its thickness can predict whether cognitively healthy (CH) individuals have a normal or pathological cerebrospinal fluid (CSF) Aß42 (A) and tau (T) ratio.
METHODS
As part of an ongoing longitudinal study, we enrolled CH individuals, excluding those with cognitive impairment and significant ocular pathology. We classified the CH group into two sub-groups, normal (CH-NAT, n = 16) or pathological (CH-PAT, n = 27), using a logistic regression model from the CSF AT ratio that identified >85% of patients with a clinically probable AD diagnosis. Spectral-domain optical coherence tomography (OCT) was acquired for RNFL, ganglion cell-inner plexiform layer (GC-IPL), and macular thickness. Group differences were tested using mixed model repeated measures and a classification model derived using multiple logistic regression.
RESULTS
Mean age (± standard deviation) in the CH-PAT group (n = 27; 75.2 ± 8.4 years) was similar (p = 0.50) to the CH-NAT group (n = 16; 74.1 ± 7.9 years). Mean RNFL (standard error) was thinner in the CH-PAT group by 9.8 (2.7) μm; p < 0.001. RNFL thickness classified CH-NAT vs. CH-PAT with 87% sensitivity and 56.3% specificity.
CONCLUSIONS
Our retinal data predict which individuals have CSF biomarkers of AD pathology before cognitive deficits are detectable with 87% sensitivity. Such results from easy-to-acquire, objective and non-invasive measurements of the RNFL merit further study of OCT technology to monitor or screen for early AD pathology.

Identifiants

pubmed: 32469871
doi: 10.1371/journal.pone.0232785
pii: PONE-D-20-02170
pmc: PMC7259639
doi:

Substances chimiques

Amyloid beta-Peptides 0
Biomarkers 0
tau Proteins 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0232785

Subventions

Organisme : NCATS NIH HHS
ID : UL1 TR001855
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005142
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG052350
Pays : United States

Commentaires et corrections

Type : ErratumIn

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Samuel Asanad (S)

Doheny Eye Institute, Los Angeles, CA, United States of America.
Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.

Michele Fantini (M)

Doheny Eye Institute, Los Angeles, CA, United States of America.
Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
Department of Medicine, Ophthalmology, University of Udine, Udine, Italy.

William Sultan (W)

Doheny Eye Institute, Los Angeles, CA, United States of America.

Marco Nassisi (M)

Doheny Eye Institute, Los Angeles, CA, United States of America.
Department of Clinical Sciences and Community Health, Ophthalmological Unit, IRCCS-Cà Granda Foundation-Ospedale Maggiore Policlinico, University of Milan, Milan, Italy.

Christian M Felix (CM)

Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.

Jessica Wu (J)

Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.

Rustum Karanjia (R)

Doheny Eye Institute, Los Angeles, CA, United States of America.
Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
Department of Ophthalmology, University of Ottawa, Ottawa, Ontario, Canada.
Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.

Fred N Ross-Cisneros (FN)

Doheny Eye Institute, Los Angeles, CA, United States of America.

Abhay P Sagare (AP)

Department of Physiology and Neuroscience, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States of America.

Berislav V Zlokovic (BV)

Department of Physiology and Neuroscience, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States of America.

Helena C Chui (HC)

Department of Neurology, University of Southern California, Los Angeles, CA, United States of America.

Janice M Pogoda (JM)

Cipher Biostatistics & Reporting, Reno, NV, United States of America.

Xianghong Arakaki (X)

Huntington Medical Research Institutes, Pasadena, CA, United States of America.

Alfred N Fonteh (AN)

Huntington Medical Research Institutes, Pasadena, CA, United States of America.

Alfredo A Sadun (AA)

Doheny Eye Institute, Los Angeles, CA, United States of America.
Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.

Michael G Harrington (MG)

Huntington Medical Research Institutes, Pasadena, CA, United States of America.

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