Carol Yim-lui Cheung1, Yi Ting Ong2, Saima Hilal3, M Kamran Ikram4, Sally Low5, Yi Lin Ong5, N Venketasubramanian6, Philip Yap7, Dennis Seow8, Christopher Li Hsian Chen9, Tien Yin Wong1. 1. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore Office of Clinical Sciences, Duke-NUS Graduate Medical School, Singapore. 2. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore. 3. Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore Memory Aging and Cognition Centre, National University Health System, Singapore Department of Pharmacology, National University of Singapore, Singapore. 4. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore Office of Clinical Sciences, Duke-NUS Graduate Medical School, Singapore Memory Aging and Cognition Centre, National University Health System, Singapore. 5. Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. 6. Memory Aging and Cognition Centre, National University Health System, Singapore. 7. Department of Geriatric Medicine, Khoo Teck Puat Hospital, Singapore. 8. Department of Geriatric Medicine, Singapore General Hospital, Singapore. 9. Memory Aging and Cognition Centre, National University Health System, Singapore Department of Pharmacology, National University of Singapore, Singapore.
Abstract
BACKGROUND: Alzheimer's disease (AD) is a neurodegenerative disorder with emerging evidence that it is associated with retinal ganglion cell loss; however, few data exist to establish this association. OBJECTIVE: To determine whether macular ganglion cell-inner plexiform layer (GC-IPL) and retinal nerve fiber layer (RNFL), as quantitatively measured by non-invasive in vivo spectral-domain optical coherence tomography (SD-OCT), are altered in patients with AD and mild cognitive impairment (MCI). METHODS: Patients with AD and MCI were recruited from dementia/memory clinics, and cognitively normal controls were selected from the Singapore Epidemiology of Eye Disease program. SD-OCT (Cirrus HD-OCT, software version 6.0.2, Carl Zeiss Meditec Inc, Dublin, CA) was used to measure the GC-IPL and RNFL thicknesses. RESULTS: Compared with cognitively normal controls (n = 123), patients with AD (n = 100) had significantly reduced GC-IPL thicknesses in all six (superior, superonasal, inferonasal, inferior, inferotemporal, and superotemporal) sectors (mean differences from -3.42 to -4.99 μm, all p < 0.05) and reduced RNFL thickness in superior quadrant (-6.04 μm, p = 0.039). Patients with MCI (n = 41) also had significantly reduced GC-IPL thicknesses compared with controls (mean differences from -3.62 to -5.83 μm, all p < 0.05). Area under receiver operating characteristic curves of GC-IPL were generally higher than that of RNFL to discriminate AD and MCI from the controls. CONCLUSIONS: Our data strengthens the link between retinal ganglion cell neuronal and optic nerve axonal loss with AD, and suggest that assessment of macular GC-IPL can be a test to detect neuronal injury in early AD and MCI.
BACKGROUND:Alzheimer's disease (AD) is a neurodegenerative disorder with emerging evidence that it is associated with retinal ganglion cell loss; however, few data exist to establish this association. OBJECTIVE: To determine whether macular ganglion cell-inner plexiform layer (GC-IPL) and retinal nerve fiber layer (RNFL), as quantitatively measured by non-invasive in vivo spectral-domain optical coherence tomography (SD-OCT), are altered in patients with AD and mild cognitive impairment (MCI). METHODS:Patients with AD and MCI were recruited from dementia/memory clinics, and cognitively normal controls were selected from the Singapore Epidemiology of Eye Disease program. SD-OCT (Cirrus HD-OCT, software version 6.0.2, Carl Zeiss Meditec Inc, Dublin, CA) was used to measure the GC-IPL and RNFL thicknesses. RESULTS: Compared with cognitively normal controls (n = 123), patients with AD (n = 100) had significantly reduced GC-IPL thicknesses in all six (superior, superonasal, inferonasal, inferior, inferotemporal, and superotemporal) sectors (mean differences from -3.42 to -4.99 μm, all p < 0.05) and reduced RNFL thickness in superior quadrant (-6.04 μm, p = 0.039). Patients with MCI (n = 41) also had significantly reduced GC-IPL thicknesses compared with controls (mean differences from -3.62 to -5.83 μm, all p < 0.05). Area under receiver operating characteristic curves of GC-IPL were generally higher than that of RNFL to discriminate AD and MCI from the controls. CONCLUSIONS: Our data strengthens the link between retinal ganglion cell neuronal and optic nerve axonal loss with AD, and suggest that assessment of macular GC-IPL can be a test to detect neuronal injury in early AD and MCI.
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