Press Release

Aging-US: Abnormalities of saccadic eye movements in dementia due to Alzheimer’s


Aging-US published a Special Collection on Eye Disease which included "Abnormalities of saccadic eye movements in dementia due to Alzheimer’s disease and mild cognitive impairment" which reported that there is increasing evidence that people in the early stages of Alzheimer’s disease 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 are at an increased likelihood of dementia due to AD.

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.

Dr. Thomas D.W. Wilcockson from The Loughborough University as well as The Lancaster University said, "Alzheimer's disease (AD) is a severe neurodegenerative disease of the human brain, for which there is as yet no cure."

When disease modifying therapy becomes available, it will be essential to administer this treatment in the very earliest stages of the disease, before pathological changes in the brain are widespread, rendering the treatment ineffective.

Figure 2. Heatmap plots of the extracted gaze signals in each of participant groups. The x-axis indicates the time since saccadic target appearance, and the y-axis presents the aligned horizontal gaze position. The warmer the colour; the higher is the gaze point density in the corresponding spatial-temporal location. Note that the longest "comet" tails, reflecting a high proportion of uncorrected errors, are evident for the Alzheimer's (AD) and the amnesic Mild Cognitive Impairment (aMCI) groups. The control participants (CP) and the non- amnesic MCI have distinctly shorter "comet" tails.

Thus, identifying the presence of AD in the pre-dementia ‘prodromal’ or even ‘preclinical’ phase is essential. Current biomarkers that are able to detect AD in the earliest stages are either invasive or expensive. A critical issue then is whether eye-movement impairments are detectable in people who are in a preclinical stage of AD and therefore at a greater risk of developing clinical dementia.

A strong correlation has been reported between antisaccade error rate with cortical thinning in a mild cognitive impairment group. However, this work did not distinguish between the different types of MCI, thus the low and high-risk of dementia participants were conflated in their study. People with a diagnosis of MCI are at an increased risk of developing dementia compared to cognitively healthy adults with 5-10% of MCI patients progressing to dementia annually.

Traditionally, the clinical syndrome of MCI was considered to be a relatively distinct stage of dementia since the cognitive deficits were not severe enough to impact significantly on the individual’s ability to conduct their activities of daily living.

The Wilcockson Research Team concluded in their Aging-US Research Output that inhibitory error rates in the antisaccade are sensitive to memory impairment, but may even precede it in a patient with dementia. The results obtained from this study demonstrate that eye movements during the AST could be used to automatically classify participants as being at a higher risk of AD. There are potentially a number of practical implications for this observation.

The results obtained from this study demonstrate that eye movements during the AST could be used to automatically classify participants as being at a higher risk of AD

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Correspondence to: Thomas D.W. Wilcockson email:

Keywords: mild cognitive impairment, Alzheimer’s disease, inhibitory control, eye tracking, anti-saccade

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.

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