![]() The OCT technique used to measure the peripapillary retinal nerve fiber layer (RNFL) and macular thickness has proven useful for the detection of significant reductions in retinal thickness in patients with AD and in those with MCI. Several studies have searched for in vivo evidence of retinal involvement in AD pathophysiology using optical coherence tomography (OCT). The accumulation of Aβ has also been reported inside and around RGCs in postmortem AD retinal specimens. Postmortem studies of AD, in addition to the well-known occurrence of neurodegeneration in the brain, have revealed a significant loss of RGCs as well as abnormal RGC dendritic morphology and size. In AD, though, the loss of retinal ganglion cells is significantly greater and is accompanied by M-cell loss. The loss or RGCs is part of the normal aging process. ![]() One of the most plausible explanations involves the loss of retinal ganglion cells (RGCs). Many patients with AD experience a loss of visual acuity, a phenomenon that has no known mechanism. Nevertheless, researchers continue to search for new, less invasive and more cost-effective biological markers of AD. Recently, there has been a remarkable growth in AD biomarkers, including cerebrospinal fluid (CSF) measurement of a lower Aβ 42 level, positron emission tomography (PET) amyloid imaging, and the assessment of medial temporal lobe atrophy via brain magnetic resonance imaging (MRI). Amnestic MCI is considered a degenerative condition that may represent prodromal AD. MCI has multiple etiologies and is categorized into amnestic and non-amnestic subtypes. The transitional phase is clinically recognized as preclinical AD and mild cognitive impairment (MCI). The pathophysiological process of AD begins many years prior to detectable cognitive impairment. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist.Īlzheimer’s disease (AD) is the most common age-related dementia and is characterized by the accumulation of amyloid-β protein (Aβ) plaques as well as aggregates of hyperphosphorylated tau as neurofibrillary tangles in the brain. 2016R1A1A1A05005484) and by the Original Technology Research Program for Brain Science through the NRF funded by the Korean government (MSIP) (No. Future interested researchers may contact the Corresponding Author( or the Inha University Hospital Institutional Data Access/Ethics committee (+82-3).įunding: This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and Future Planning (No. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: Due to ethical restrictions, an anonymized minimal dataset will be available upon request. Received: Accepted: AugPublished: September 6, 2016Ĭopyright: © 2016 Choi et al. PLoS ONE 11(9):Įditor: Thomas Arendt, Universitatsklinikum Leipzig, GERMANY Citation: Choi SH, Park SJ, Kim NR (2016) Macular Ganglion Cell -Inner Plexiform Layer Thickness Is Associated with Clinical Progression in Mild Cognitive Impairment and Alzheimers Disease.
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