Saccade deficits in amnestic mild cognitive impairment resemble mild Alzheimer's disease

Alzheimer's disease (AD) is a disorder of progressive memory loss and executive dysfunction. Little is known about the progression from amnestic mild cognitive impairment (aMCI; isolated memory loss) to AD. Studies have found impairments in mild‐stage AD and aMCI in specific tests of executive...

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Veröffentlicht in:The European journal of neuroscience 2014-06, Vol.39 (11), p.2000-2013
Hauptverfasser: Peltsch, Alicia, Hemraj, Alisha, Garcia, Angeles, Munoz, Douglas P.
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container_end_page 2013
container_issue 11
container_start_page 2000
container_title The European journal of neuroscience
container_volume 39
creator Peltsch, Alicia
Hemraj, Alisha
Garcia, Angeles
Munoz, Douglas P.
description Alzheimer's disease (AD) is a disorder of progressive memory loss and executive dysfunction. Little is known about the progression from amnestic mild cognitive impairment (aMCI; isolated memory loss) to AD. Studies have found impairments in mild‐stage AD and aMCI in specific tests of executive function. Here, we used objective saccade tasks to determine if they can effectively assess executive function deficits otherwise assessed by neuropsychological testing. To determine which executive function deficits the saccade tasks are most sensitive to, we also investigated the relationship between performance on saccade tasks and neuropsychological test scores. Twenty‐two aMCI patients (63–90 years), 24 mild AD patients (61–87 years) and 76 healthy controls (60–85 years) performed a battery of neuropsychological tests, and two saccade tasks designed to probe sensory, motor and cognitive function. The prosaccade task requires a fast, automatic saccade toward an eccentric visual stimulus. The antisaccade task requires additional executive processing to inhibit the automatic prosaccade toward the stimulus, so that a voluntary saccade can be initiated to a location opposite the stimulus. Antisaccade performance was impaired similarly in aMCI and AD patients relative to controls; both groups were slower to initiate correct antisaccades and they made more direction errors (erroneous prosaccades), suggesting similar brain deficits. Scores on the Stroop task were inversely correlated with the percentage of short‐latency direction errors in the antisaccade task for controls and aMCI patients, whereas other more global measures of executive function were not related to saccade measures in any subject group. Our results show that the antisaccade task is useful for detecting executive dysfunction in aMCI and AD, especially dysfunction in selective attention. Saccade tasks may therefore have potential to assess executive dysfunction when use of neuropsychological tests is not possible. The prosaccade task (look toward a peripheral stimulus) and antisaccade task (inhibit prosaccade to peripheral stimulus and instead initiate saccade to opposite location) are used to assess cognitive impairment. Disease‐specific patterns begin to emerge. Individual antisaccade traces for a representative 75 year old elderly control, a 76 year old aMCI patient, and a 75 year old AD patient are shown here. Solid lines = correct saccades, dotted lines = direction errors. S = stimulus, FP = fixati
doi_str_mv 10.1111/ejn.12617
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Little is known about the progression from amnestic mild cognitive impairment (aMCI; isolated memory loss) to AD. Studies have found impairments in mild‐stage AD and aMCI in specific tests of executive function. Here, we used objective saccade tasks to determine if they can effectively assess executive function deficits otherwise assessed by neuropsychological testing. To determine which executive function deficits the saccade tasks are most sensitive to, we also investigated the relationship between performance on saccade tasks and neuropsychological test scores. Twenty‐two aMCI patients (63–90 years), 24 mild AD patients (61–87 years) and 76 healthy controls (60–85 years) performed a battery of neuropsychological tests, and two saccade tasks designed to probe sensory, motor and cognitive function. The prosaccade task requires a fast, automatic saccade toward an eccentric visual stimulus. The antisaccade task requires additional executive processing to inhibit the automatic prosaccade toward the stimulus, so that a voluntary saccade can be initiated to a location opposite the stimulus. Antisaccade performance was impaired similarly in aMCI and AD patients relative to controls; both groups were slower to initiate correct antisaccades and they made more direction errors (erroneous prosaccades), suggesting similar brain deficits. Scores on the Stroop task were inversely correlated with the percentage of short‐latency direction errors in the antisaccade task for controls and aMCI patients, whereas other more global measures of executive function were not related to saccade measures in any subject group. Our results show that the antisaccade task is useful for detecting executive dysfunction in aMCI and AD, especially dysfunction in selective attention. Saccade tasks may therefore have potential to assess executive dysfunction when use of neuropsychological tests is not possible. The prosaccade task (look toward a peripheral stimulus) and antisaccade task (inhibit prosaccade to peripheral stimulus and instead initiate saccade to opposite location) are used to assess cognitive impairment. Disease‐specific patterns begin to emerge. Individual antisaccade traces for a representative 75 year old elderly control, a 76 year old aMCI patient, and a 75 year old AD patient are shown here. Solid lines = correct saccades, dotted lines = direction errors. S = stimulus, FP = fixation point.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>aging</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Amnesia - physiopathology</subject><subject>Case-Control Studies</subject><subject>Cognitive Dysfunction - physiopathology</subject><subject>dementia</subject><subject>Executive Function</subject><subject>eye movements</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Psychomotor Performance</subject><subject>Reaction Time</subject><subject>saccade</subject><subject>Saccades</subject><subject>Stroop Test</subject><issn>0953-816X</issn><issn>1460-9568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1P3DAQhi1UBFvg0D9Q5VZ6CHhix3aOiK8WrQCprbriYvlj0prG2cXOtqW_vikBbpWYy1ye95nRS8gboAcwziHe9gdQCZAbZAZc0LKphXpFZrSpWalALLbJ65xvKaVK8HqLbFdcNZRLmJHFJ-Oc8Vh4bIMLQy5CX5jYYx6CK2LofOGW3_owhJ9YhLgyIUXshyJhxmg7nJCj7s93DBHTu1z4kNFk3CWbreky7j3uHfLl7PTz8YdyfnX-8fhoXjouKllyqIyhyoBoqJLOtxYck1Q4qwxFC2BBYmNrj8Ckt2iYaaEWVjXMYeNbtkP2J-8qLe_W49s6huyw60yPy3XWUHNaVXw89gKUVVxKqcSIvp9Ql5Y5J2z1KoVo0r0Gqv91rsfO9UPnI_v2Ubu2Ef0z-VTyCBxOwK_Q4f3_Tfr04vJJWU6JkAf8_Zww6YcWkslaf70819XF9fxkcXaj5-wvXqea-A</recordid><startdate>201406</startdate><enddate>201406</enddate><creator>Peltsch, Alicia</creator><creator>Hemraj, Alisha</creator><creator>Garcia, Angeles</creator><creator>Munoz, Douglas P.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>201406</creationdate><title>Saccade deficits in amnestic mild cognitive impairment resemble mild Alzheimer's disease</title><author>Peltsch, Alicia ; Hemraj, Alisha ; Garcia, Angeles ; Munoz, Douglas P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4627-412aa08a169087cdfb1c3706cb8a0eb11b17e9b5de137dbea3af156b893ce9df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>aging</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Amnesia - physiopathology</topic><topic>Case-Control Studies</topic><topic>Cognitive Dysfunction - physiopathology</topic><topic>dementia</topic><topic>Executive Function</topic><topic>eye movements</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Psychomotor Performance</topic><topic>Reaction Time</topic><topic>saccade</topic><topic>Saccades</topic><topic>Stroop Test</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Peltsch, Alicia</creatorcontrib><creatorcontrib>Hemraj, Alisha</creatorcontrib><creatorcontrib>Garcia, Angeles</creatorcontrib><creatorcontrib>Munoz, Douglas P.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>The European journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Peltsch, Alicia</au><au>Hemraj, Alisha</au><au>Garcia, Angeles</au><au>Munoz, Douglas P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Saccade deficits in amnestic mild cognitive impairment resemble mild Alzheimer's disease</atitle><jtitle>The European journal of neuroscience</jtitle><addtitle>Eur J Neurosci</addtitle><date>2014-06</date><risdate>2014</risdate><volume>39</volume><issue>11</issue><spage>2000</spage><epage>2013</epage><pages>2000-2013</pages><issn>0953-816X</issn><eissn>1460-9568</eissn><abstract>Alzheimer's disease (AD) is a disorder of progressive memory loss and executive dysfunction. Little is known about the progression from amnestic mild cognitive impairment (aMCI; isolated memory loss) to AD. Studies have found impairments in mild‐stage AD and aMCI in specific tests of executive function. Here, we used objective saccade tasks to determine if they can effectively assess executive function deficits otherwise assessed by neuropsychological testing. To determine which executive function deficits the saccade tasks are most sensitive to, we also investigated the relationship between performance on saccade tasks and neuropsychological test scores. Twenty‐two aMCI patients (63–90 years), 24 mild AD patients (61–87 years) and 76 healthy controls (60–85 years) performed a battery of neuropsychological tests, and two saccade tasks designed to probe sensory, motor and cognitive function. The prosaccade task requires a fast, automatic saccade toward an eccentric visual stimulus. The antisaccade task requires additional executive processing to inhibit the automatic prosaccade toward the stimulus, so that a voluntary saccade can be initiated to a location opposite the stimulus. Antisaccade performance was impaired similarly in aMCI and AD patients relative to controls; both groups were slower to initiate correct antisaccades and they made more direction errors (erroneous prosaccades), suggesting similar brain deficits. Scores on the Stroop task were inversely correlated with the percentage of short‐latency direction errors in the antisaccade task for controls and aMCI patients, whereas other more global measures of executive function were not related to saccade measures in any subject group. Our results show that the antisaccade task is useful for detecting executive dysfunction in aMCI and AD, especially dysfunction in selective attention. Saccade tasks may therefore have potential to assess executive dysfunction when use of neuropsychological tests is not possible. The prosaccade task (look toward a peripheral stimulus) and antisaccade task (inhibit prosaccade to peripheral stimulus and instead initiate saccade to opposite location) are used to assess cognitive impairment. Disease‐specific patterns begin to emerge. Individual antisaccade traces for a representative 75 year old elderly control, a 76 year old aMCI patient, and a 75 year old AD patient are shown here. Solid lines = correct saccades, dotted lines = direction errors. S = stimulus, FP = fixation point.</abstract><cop>France</cop><pub>Blackwell Publishing Ltd</pub><pmid>24890471</pmid><doi>10.1111/ejn.12617</doi><tpages>14</tpages></addata></record>
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subjects Aged
Aged, 80 and over
aging
Alzheimer Disease - physiopathology
Amnesia - physiopathology
Case-Control Studies
Cognitive Dysfunction - physiopathology
dementia
Executive Function
eye movements
Female
Humans
Male
Middle Aged
Psychomotor Performance
Reaction Time
saccade
Saccades
Stroop Test
title Saccade deficits in amnestic mild cognitive impairment resemble mild Alzheimer's disease
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