Retinal thickness in patients with mild cognitive impairment and Alzheimer's disease

Abstract Objectives Mild cognitive impairment (MCI) may represent a transition to early Alzheimer's disease (AD). The retinal nerve fiber layer (RNFL) is composed of axons originating in retinal ganglion cells that eventually form the optic nerves. Previous studies have shown that degenerative...

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Published inClinical neurology and neurosurgery Vol. 113; no. 7; pp. 523 - 526
Main Authors Kesler, Anat, Vakhapova, Veronika, Korczyn, Amos D, Naftaliev, Elvira, Neudorfer, Meira
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 01.09.2011
Elsevier
Elsevier Limited
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Summary:Abstract Objectives Mild cognitive impairment (MCI) may represent a transition to early Alzheimer's disease (AD). The retinal nerve fiber layer (RNFL) is composed of axons originating in retinal ganglion cells that eventually form the optic nerves. Previous studies have shown that degenerative changes occur in optic nerve fibers and manifested as thinning of RNFL in patients with AD. The objective of this study was to assess the relationship between MCI, AD and loss of RNFL. Patients and methods In this study, patients fulfilling diagnostic criteria for MCI ( n = 24), AD ( n = 30) and cognitively normal age-matched controls ( n = 24) have undergone neuro-ophthalmologic and optical coherence tomography (OCT) examinations to measure RNFL thickness. Results There was a significant decrease in RNFL thickness in both study groups (AD and MCI) compared to the control group, particularly in the inferior quadrants of the optic nerve head, while the superior quadrants were significantly thinner only in AD. Although AD patients may have more severe changes than MCI cases, the differences were statistically nonsignificant. Furthermore among AD patients, there was no relation to the severity of the dementia. Conclusions Our data confirm the retinal involvement in AD, as reflected by loss of axons in the optic nerves.
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ISSN:0303-8467
1872-6968
DOI:10.1016/j.clineuro.2011.02.014