Retinal thickness in Alzheimer's disease: A systematic review and meta‐analysis

Haan, Jurre den; Verbraak, Frank D.; Visser, Pieter Jelle; Bouwman, Femke H.

doi:10.1016/j.dadm.2016.12.014

Cited by 166 publications

(145 citation statements)

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“…These results provide an in vivo validation for that which was previously observed ex vivo by Perez et al 44 In future studies, the inner and outer retina could be subdivided further to quantify individual layer thickness. Since RNFL thinning occurs in AD patients, 28,29 it may also be interesting to quantify the RNFL thickness alone in this mouse model. However, quantifying the RNFL thickness in mice using OCT is difficult, as the peripapillary thickness of the healthy RNFL is only approximately 20 µm, 74 and is interrupted by blood vessels and ganglion cells.…”

Section: Cortical Amyloid Beta Plaque Loadmentioning

confidence: 99%

“…26,27 Retinal layer thinning, particularly in the retinal nerve fiber layer (RNFL), is also present in the retina of AD patients. 28,29 However looking forward to a marker for diagnosis, RNFL thinning is not specific to AD and it is not only associated with other diseases such as glaucoma 30 and Parkinson's disease, 31 but also more generally with increasing age. 32 With many contradictory observations, it is clear that there is still a great deal of research to be performed in order to fully understand the effects of AD on the retina.…”

Section: Introductionmentioning

confidence: 99%

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Retinal analysis of a mouse model of Alzheimer’s disease with multicontrast optical coherence tomography

et al. 2020

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Recent Alzheimer's disease (AD) patient studies have focused on retinal analysis, as the retina is the only part of the central nervous system which can be imaged non-invasively by optical methods. However as this is a relatively new approach, the occurrence and role of pathological features such as retinal layer thinning, extracellular amyloid beta (Aβ) accumulation and vascular changes is still debated. Animal models of AD are therefore often used in attempts to understand the disease. In this work, both eyes of 24 APP/PS1 transgenic mice (age: 45-104 weeks) and 15 age-matched wildtype littermates were imaged by a custom-built multi-contrast optical coherence tomography (OCT) system. The system provided a combination of standard reflectivity data, polarization-sensitive data and OCT angiograms. This tri-fold contrast provided qualitative and quantitative information on retinal layer thickness and structure, presence of hyper-reflective foci, phase retardation abnormalities and retinal vasculature. While abnormal structural properties and phase retardation signals were observed in the retinas, the observations were very similar in transgenic and control mice. At the end of the experiment, retinas and brains were harvested from a subset of the mice (14 transgenic, 7 age-matched control) in order to compare the in vivo results to histological analysis, and to quantify the cortical Aβ plaque load. arXiv:1909.08466v2 [physics.med-ph]

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Section: Cortical Amyloid Beta Plaque Loadmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Retinal analysis of a mouse model of Alzheimer’s disease with multicontrast optical coherence tomography

et al. 2020

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“…Истончение комплекса ГКС и СНВС описано при болезни Альцгеймера [24] и болезни Паркинсона [25]. По данным метаанализа, включавшего 25 исследований, 887 пациентов, при болезни Альцгеймера отмечается общее снижение толщины СНВС, максимально выраженное в верхнем и нижнем квадрантах [26]. Установлено также снижение толщины сетчатки во всех отделах макулярной зоны с максимальным истончением в периферических отделах, относящихся к магноцеллюлярной системе [26].…”

Section: Discussionunclassified

“…По данным метаанализа, включавшего 25 исследований, 887 пациентов, при болезни Альцгеймера отмечается общее снижение толщины СНВС, максимально выраженное в верхнем и нижнем квадрантах [26]. Установлено также снижение толщины сетчатки во всех отделах макулярной зоны с максимальным истончением в периферических отделах, относящихся к магноцеллюлярной системе [26]. Подобный паттерн атрофии клеток отмечают при глаукоме [27,28], сходство в патогенезе данных заболеваний подтверждают и другие исследования [29,30].…”

Section: Discussionunclassified

Retinal and choroidal morphological changes in Huntington's disease

Светозарский

Kopishinskaia

Сметанкин

2019

Rossijskij oftalʹmologičeskij žurnal

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Purpose: to investigate the choroidal and retinal morphology in Huntington's disease (HD) using optical coherence tomography (OCT) and to analyze how the parameters studied correlate with the clinical data. Material and methods. The study included two groups of subjects, (1) 44 HD patients, averagely aged 37.6 ± 10.2 yrs, and (2) 31 healthy volunteers, averagely aged 37.3 ± 10.8 yrs. The groups had matching age, sex distribution, intraocular pressure and mean refractive error. In the study group, 21 patients had pre-manifest and 23, manifest HD stage. All patients underwent a thorough neurological and ophthalmic examination which included retinal OCT. The foveal choroidal thickness, retinal thickness in 9 areas of the macular zone, retinal ganglion cells complex (GCC) and peripapillary retinal nerve fiber layer thickness (RNFL) were evaluated in 4 quadrants. CAG repeat expansion size (cytosine-adenine-guanine) in the huntingtin gene, the disease duration and Unified HD Rating Scale motor scores (UHDRS) were evaluated for HD patients. Results. The range of the CAG repeat expansion size in the study group was 37–56 repeats (44.3 ± 3.8), the UHDRS motor score was 36.3 ± 29.7, disease duration was 13.7 ± 7.2 years. OCT revealed a significant decrease in the foveal choroidal thickness, GCC complex thickness, average, temporal, inferior and nasal RNFL thickness and total retinal thickness in the external temporal area in HD patients as compared to the controls. In addition, an inverse correlation between the disease duration, UHDRS Motor Score and a number of OCT parameters was found. Conclusion. The results confirm the promising potential of retinal tomographic parameters as a biomarker for early diagnosis and monitoring of the neurodegenerative process progression. The topography of retinal thickness reduction indicates a specific pattern of retinal neurodegeneration in HD.

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“…Other biomarkers of AD were studied based on the hypothesis that AD is a vascular disorder [10]. Alternative biomarkers were also put forward, like the thinning of the retinal nerve fibre layer (RNFL) in the eyes of AD patients [11,12]. Here, a particularly confounding factor is the fact that RNFL thinning is not exclusive to AD [13].…”

Section: Introductionmentioning

confidence: 99%

Characterization of the retinal changes of the 3×Tg-AD mouse model of Alzheimer’s disease

et al. 2020

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder whose diagnosis remains a notable challenge. The literature suggests that cerebral changes precede AD symptoms by over two decades, implying a significantly advanced stage of AD by the time it is usually diagnosed. In the study herein, texture analysis was applied to computed optical coherence tomography ocular fundus images to identify differences between a group of the transgenic mouse model of the Alzheimer's disease (3×Tg-AD) and a group of wild-type mice, at the ages of one and two-months-old. A substantial difference between groups was found at both time-points across all neuroretina's layers. Here, the inner nuclear layer stands out both in the level of statistically significant differences and on the extension of these differences which span through the imaged area. Also, the progression of AD is suggested to be spotted by texture analysis as demonstrated by the significant difference found in the inner plexiform and the outer nuclear layers from the age of one to the age of two-months-old. These findings demonstrate the potential of the use of the retina and texture analysis to the diagnosis of AD and monitor AD progression. Besides, the differences between groups found in this study suggest that the 3×Tg-AD model may be inappropriate to study early changes associated with the AD and other animal models should be tested following the same path and rationale. Moreover, these results also suggest that the human genes present in these transgenic mice may have an impact on the neurodevelopment of offspring which would justify the significant changes found at the age of one-month-old.

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Retinal thickness in Alzheimer's disease: A systematic review and meta‐analysis

Cited by 166 publications

References 50 publications

Retinal analysis of a mouse model of Alzheimer’s disease with multicontrast optical coherence tomography

Retinal analysis of a mouse model of Alzheimer’s disease with multicontrast optical coherence tomography

Retinal and choroidal morphological changes in Huntington's disease

Characterization of the retinal changes of the 3×Tg-AD mouse model of Alzheimer’s disease

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