Cerebrovascular Reactivity Impairment in Preclinical Alzheimer's Disease

ABSTRACT BACKGROUND AND PURPOSE A substantial overlap exists between declines in cerebral vasoreactivity (CVR) and symptomatic Alzheimer's disease (AD). CVR can be quantified using transcranial Doppler (TCD) measurement of cerebral blood flow velocities (CBFV) in the middle cerebral artery (MCA...

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Veröffentlicht in:Journal of neuroimaging 2019-07, Vol.29 (4), p.493-498
Hauptverfasser: Alwatban, Mohammed, Murman, Daniel L., Bashford, Greg
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Murman, Daniel L.
Bashford, Greg
description ABSTRACT BACKGROUND AND PURPOSE A substantial overlap exists between declines in cerebral vasoreactivity (CVR) and symptomatic Alzheimer's disease (AD). CVR can be quantified using transcranial Doppler (TCD) measurement of cerebral blood flow velocities (CBFV) in the middle cerebral artery (MCA) with CO2 as a vasodilatory stimulus. The breath‐hold acceleration index (BHAI) is a new, more reliable measure of CVR developed recently in our laboratory. Our primary goal is to explore the possibility of using TCD for asymptomatic AD screening. METHODS A pilot study population was divided into three groups: 9 healthy control subjects, 8 subjects identified as preclinical AD, and 10 patients diagnosed with prodromal or mild AD. Control subjects had a Clinical Dementia Rating (CDR) score of 0 without elevated amyloid‐β (Aβ) on amyloid positron emission tomography (PET) imaging, preclinical AD subjects had CDR = 0 with elevated Aβ, and prodromal to mild AD subjects had CDR scores ≥.5 and elevated Aβ. CVR was calculated using two indices: the conventional breath‐holding index (BHI) and the new BHAI. TCD parameters between the three groups were compared. RESULTS BHAI was able to distinguish between 9 normal control subjects and 8 preclinical‐AD subjects with high statistical significance (P 
doi_str_mv 10.1111/jon.12606
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CVR can be quantified using transcranial Doppler (TCD) measurement of cerebral blood flow velocities (CBFV) in the middle cerebral artery (MCA) with CO2 as a vasodilatory stimulus. The breath‐hold acceleration index (BHAI) is a new, more reliable measure of CVR developed recently in our laboratory. Our primary goal is to explore the possibility of using TCD for asymptomatic AD screening. METHODS A pilot study population was divided into three groups: 9 healthy control subjects, 8 subjects identified as preclinical AD, and 10 patients diagnosed with prodromal or mild AD. Control subjects had a Clinical Dementia Rating (CDR) score of 0 without elevated amyloid‐β (Aβ) on amyloid positron emission tomography (PET) imaging, preclinical AD subjects had CDR = 0 with elevated Aβ, and prodromal to mild AD subjects had CDR scores ≥.5 and elevated Aβ. CVR was calculated using two indices: the conventional breath‐holding index (BHI) and the new BHAI. TCD parameters between the three groups were compared. RESULTS BHAI was able to distinguish between 9 normal control subjects and 8 preclinical‐AD subjects with high statistical significance (P &lt; .001). BHI and pulsatility index were able only to distinguish AD from healthy and preclinical subjects (P &lt; .001). CONCLUSIONS In this exploratory pilot study, CVR was significantly decreased in preclinical, prodromal, and mild AD subjects as compared to the healthy group. Lower CVR in the preclinical AD group was detected using the new BHAI index but not the conventional BHI index.</description><identifier>ISSN: 1051-2284</identifier><identifier>EISSN: 1552-6569</identifier><identifier>DOI: 10.1111/jon.12606</identifier><identifier>PMID: 30748053</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Acceleration ; Alzheimer's disease ; Amyloid ; Blood flow ; breath‐holding index ; Carbon dioxide ; Cerebral blood flow ; cerebrovascular reactivity ; Dementia disorders ; Neurodegenerative diseases ; Neuroimaging ; Population (statistical) ; Population studies ; Positron emission ; Positron emission tomography ; preclinical Alzheimer's diseases ; Tomography ; transcranial Doppler ultrasound ; Ultrasound</subject><ispartof>Journal of neuroimaging, 2019-07, Vol.29 (4), p.493-498</ispartof><rights>2019 by the American Society of Neuroimaging</rights><rights>2019 by the American Society of Neuroimaging.</rights><rights>2019 American Society of Neuroimaging</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4196-efb6c5e054856c2b2c391afc278e15087258c362e7113116436a71b8eb72c8093</citedby><cites>FETCH-LOGICAL-c4196-efb6c5e054856c2b2c391afc278e15087258c362e7113116436a71b8eb72c8093</cites><orcidid>0000-0003-0184-1533</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjon.12606$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjon.12606$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30748053$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alwatban, Mohammed</creatorcontrib><creatorcontrib>Murman, Daniel L.</creatorcontrib><creatorcontrib>Bashford, Greg</creatorcontrib><title>Cerebrovascular Reactivity Impairment in Preclinical Alzheimer's Disease</title><title>Journal of neuroimaging</title><addtitle>J Neuroimaging</addtitle><description>ABSTRACT BACKGROUND AND PURPOSE A substantial overlap exists between declines in cerebral vasoreactivity (CVR) and symptomatic Alzheimer's disease (AD). CVR can be quantified using transcranial Doppler (TCD) measurement of cerebral blood flow velocities (CBFV) in the middle cerebral artery (MCA) with CO2 as a vasodilatory stimulus. The breath‐hold acceleration index (BHAI) is a new, more reliable measure of CVR developed recently in our laboratory. Our primary goal is to explore the possibility of using TCD for asymptomatic AD screening. METHODS A pilot study population was divided into three groups: 9 healthy control subjects, 8 subjects identified as preclinical AD, and 10 patients diagnosed with prodromal or mild AD. Control subjects had a Clinical Dementia Rating (CDR) score of 0 without elevated amyloid‐β (Aβ) on amyloid positron emission tomography (PET) imaging, preclinical AD subjects had CDR = 0 with elevated Aβ, and prodromal to mild AD subjects had CDR scores ≥.5 and elevated Aβ. CVR was calculated using two indices: the conventional breath‐holding index (BHI) and the new BHAI. TCD parameters between the three groups were compared. RESULTS BHAI was able to distinguish between 9 normal control subjects and 8 preclinical‐AD subjects with high statistical significance (P &lt; .001). BHI and pulsatility index were able only to distinguish AD from healthy and preclinical subjects (P &lt; .001). CONCLUSIONS In this exploratory pilot study, CVR was significantly decreased in preclinical, prodromal, and mild AD subjects as compared to the healthy group. Lower CVR in the preclinical AD group was detected using the new BHAI index but not the conventional BHI index.</description><subject>Acceleration</subject><subject>Alzheimer's disease</subject><subject>Amyloid</subject><subject>Blood flow</subject><subject>breath‐holding index</subject><subject>Carbon dioxide</subject><subject>Cerebral blood flow</subject><subject>cerebrovascular reactivity</subject><subject>Dementia disorders</subject><subject>Neurodegenerative diseases</subject><subject>Neuroimaging</subject><subject>Population (statistical)</subject><subject>Population studies</subject><subject>Positron emission</subject><subject>Positron emission tomography</subject><subject>preclinical Alzheimer's diseases</subject><subject>Tomography</subject><subject>transcranial Doppler ultrasound</subject><subject>Ultrasound</subject><issn>1051-2284</issn><issn>1552-6569</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp10D1PwzAQBmALgWgpDPwBFIkBGEJ9Tuw4Y1U-WlRRhGCOHHMVrvJR7KSo_HoMKQxIeDkPz706vYQcA70E_4bLuroEJqjYIX3gnIWCi3TX_ymHkDEZ98iBc0tKGcQs2ie9iCaxpDzqk8kYLea2Xiun20LZ4BGVbszaNJtgWq6UsSVWTWCq4MGiLkxltCqCUfHxiqZEe-aCK-NQOTwkewtVODzazgF5vrl-Gk_C2fx2Oh7NQh1DKkJc5EJzpDyWXGiWMx2loBaaJRKBU5kwLnUkGCYAEYCII6ESyCXmCdOSptGAnHe5K1u_teiarDROY1GoCuvWZYyxlKZCSvD09A9d1q2t_HVecRCUUoi9uuiUtrVzFhfZyppS2U0GNPuq129V2Xe93p5sE9u8xJdf-dOnB8MOvJsCN_8nZXfz-y7yEyezgeM</recordid><startdate>201907</startdate><enddate>201907</enddate><creator>Alwatban, Mohammed</creator><creator>Murman, Daniel L.</creator><creator>Bashford, Greg</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7QP</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0184-1533</orcidid></search><sort><creationdate>201907</creationdate><title>Cerebrovascular Reactivity Impairment in Preclinical Alzheimer's Disease</title><author>Alwatban, Mohammed ; Murman, Daniel L. ; Bashford, Greg</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4196-efb6c5e054856c2b2c391afc278e15087258c362e7113116436a71b8eb72c8093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Acceleration</topic><topic>Alzheimer's disease</topic><topic>Amyloid</topic><topic>Blood flow</topic><topic>breath‐holding index</topic><topic>Carbon dioxide</topic><topic>Cerebral blood flow</topic><topic>cerebrovascular reactivity</topic><topic>Dementia disorders</topic><topic>Neurodegenerative diseases</topic><topic>Neuroimaging</topic><topic>Population (statistical)</topic><topic>Population studies</topic><topic>Positron emission</topic><topic>Positron emission tomography</topic><topic>preclinical Alzheimer's diseases</topic><topic>Tomography</topic><topic>transcranial Doppler ultrasound</topic><topic>Ultrasound</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alwatban, Mohammed</creatorcontrib><creatorcontrib>Murman, Daniel L.</creatorcontrib><creatorcontrib>Bashford, Greg</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuroimaging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alwatban, Mohammed</au><au>Murman, Daniel L.</au><au>Bashford, Greg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cerebrovascular Reactivity Impairment in Preclinical Alzheimer's Disease</atitle><jtitle>Journal of neuroimaging</jtitle><addtitle>J Neuroimaging</addtitle><date>2019-07</date><risdate>2019</risdate><volume>29</volume><issue>4</issue><spage>493</spage><epage>498</epage><pages>493-498</pages><issn>1051-2284</issn><eissn>1552-6569</eissn><abstract>ABSTRACT BACKGROUND AND PURPOSE A substantial overlap exists between declines in cerebral vasoreactivity (CVR) and symptomatic Alzheimer's disease (AD). CVR can be quantified using transcranial Doppler (TCD) measurement of cerebral blood flow velocities (CBFV) in the middle cerebral artery (MCA) with CO2 as a vasodilatory stimulus. The breath‐hold acceleration index (BHAI) is a new, more reliable measure of CVR developed recently in our laboratory. Our primary goal is to explore the possibility of using TCD for asymptomatic AD screening. METHODS A pilot study population was divided into three groups: 9 healthy control subjects, 8 subjects identified as preclinical AD, and 10 patients diagnosed with prodromal or mild AD. Control subjects had a Clinical Dementia Rating (CDR) score of 0 without elevated amyloid‐β (Aβ) on amyloid positron emission tomography (PET) imaging, preclinical AD subjects had CDR = 0 with elevated Aβ, and prodromal to mild AD subjects had CDR scores ≥.5 and elevated Aβ. CVR was calculated using two indices: the conventional breath‐holding index (BHI) and the new BHAI. TCD parameters between the three groups were compared. RESULTS BHAI was able to distinguish between 9 normal control subjects and 8 preclinical‐AD subjects with high statistical significance (P &lt; .001). BHI and pulsatility index were able only to distinguish AD from healthy and preclinical subjects (P &lt; .001). CONCLUSIONS In this exploratory pilot study, CVR was significantly decreased in preclinical, prodromal, and mild AD subjects as compared to the healthy group. Lower CVR in the preclinical AD group was detected using the new BHAI index but not the conventional BHI index.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30748053</pmid><doi>10.1111/jon.12606</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0003-0184-1533</orcidid></addata></record>
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subjects Acceleration
Alzheimer's disease
Amyloid
Blood flow
breath‐holding index
Carbon dioxide
Cerebral blood flow
cerebrovascular reactivity
Dementia disorders
Neurodegenerative diseases
Neuroimaging
Population (statistical)
Population studies
Positron emission
Positron emission tomography
preclinical Alzheimer's diseases
Tomography
transcranial Doppler ultrasound
Ultrasound
title Cerebrovascular Reactivity Impairment in Preclinical Alzheimer's Disease
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