Abnormalities of saccadic eye movements in dementia due to Alzheimer's disease and mild cognitive impairment.

Thomas D.W Wilcockson,Rebecca Killick,Trevor J Crawford,Simon Taylor,Ira Leroi,Baiqiang Xia,Hans W Gellersen,Diako Mardanbegi,Pete Sawyer

doi:10.18632/aging.102118

Abstract

Background: There is increasing evidence that people in the early stages of Alzheimer’s disease (AD) have subtle impairments in cognitive inhibition that can be detected by using relatively simple eye-tracking paradigms, but these subtle impairments are often missed by traditional cognitive assessments. People with mild cognitive impairment (MCI) are at an increased likelihood of dementia due to AD. No study has yet investigated and contrasted the MCI subtypes in relation to eye movement performance. Methods: In this work we explore whether eye-tracking impairments can distinguish between patients with the amnesic and the non-amnesic variants of MCI. Participants were 68 people with dementia due to AD, 42 had a diagnosis of aMCI, and 47 had a diagnosis of naMCI, and 92 age-matched cognitively healthy controls. Results: The findings revealed that eye-tracking can distinguish between the two forms of MCI. Conclusions: The work provides further support for eye-tracking as a useful diagnostic biomarker in the assessment of dementia.

Highlights

Alzheimer's disease (AD) is a severe neurodegenerative disease of the human brain, for which there is as yet no cure
Alzheimer’s disease (AD) (N=65; mean=404; SD=86; 95% CI=383-427) generated significantly longer latencies than the CP group (N=91; mean=338ms; SD=84; 95% CI=321 -355; t(154)=4.801;p
We can summarise the key findings from this work: (1) These findings demonstrate for the first time, that the antisaccade task (AST) can discriminate between people with amnesic MCI (aMCI) and naMCI; and (2) The findings replicated the previously reported impairment in inhibitory control of antisaccades in people with dementia due to AD

Summary

Introduction

Alzheimer's disease (AD) is a severe neurodegenerative disease of the human brain, for which there is as yet no cure. The inhibition of a gaze-shift towards a salient stimulus as well as the ability to direct a voluntary gaze-shift away from this stimulus is impaired This difficulty in gaze control may be due to cognitive defects of either inhibitory control, working memory (WM), or both [6,7]. A critical issue is whether eye-movement impairments are detectable in people who are in a preclinical stage of AD and at a greater risk of developing clinical dementia. There is increasing evidence that people in the early stages of Alzheimer’s disease (AD) have subtle impairments in cognitive inhibition that can be detected by using relatively simple eye-tracking paradigms, but these subtle impairments are often missed by traditional cognitive assessments. Conclusions: The work provides further support for eyetracking as a useful diagnostic biomarker in the assessment of dementia

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Results

Conclusion