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Dementia: new vistas and opportunities
Over the past four decades, Alzheimer disease has become near synonymous with dementia and the amyloid/tau hypothesis as its dominant explanation. However, this monorail approach to etiology has failed to yield a single disease-modifying drug. Part of the explanation stems from the fact that most de...
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Published in: | Neurological sciences 2019-04, Vol.40 (4), p.763-767 |
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description | Over the past four decades, Alzheimer disease has become near synonymous with dementia and the amyloid/tau hypothesis as its dominant explanation. However, this monorail approach to etiology has failed to yield a single disease-modifying drug. Part of the explanation stems from the fact that most dementias in the elderly result from interactive Alzheimer and cerebrovascular pathologies. Stroke and dementia share the same risk factors and their control is associated with a decrease in stroke and some dementias. Additionally, intensive control of risk factors and enhancement of protective factors improve cognition. Moreover, anticoagulation of atrial fibrillation patients decreases their chance of developing dementia by 48%. Preliminary data suggest that treating blood pressure to a target of 120 mmHg systolic compared to a target of 140 mmHg decreases the chances of mild cognitive impairment by 19%. The Berlin Manifesto establishes the scientific bases of “preventing dementia by preventing stroke.” Enlarging our vista of dementia to include cerebrovascular disease offers the opportunity of preventing not only stroke, but some dementias, beginning now. |
doi_str_mv | 10.1007/s10072-019-3714-1 |
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However, this monorail approach to etiology has failed to yield a single disease-modifying drug. Part of the explanation stems from the fact that most dementias in the elderly result from interactive Alzheimer and cerebrovascular pathologies. Stroke and dementia share the same risk factors and their control is associated with a decrease in stroke and some dementias. Additionally, intensive control of risk factors and enhancement of protective factors improve cognition. Moreover, anticoagulation of atrial fibrillation patients decreases their chance of developing dementia by 48%. Preliminary data suggest that treating blood pressure to a target of 120 mmHg systolic compared to a target of 140 mmHg decreases the chances of mild cognitive impairment by 19%. The Berlin Manifesto establishes the scientific bases of “preventing dementia by preventing stroke.” Enlarging our vista of dementia to include cerebrovascular disease offers the opportunity of preventing not only stroke, but some dementias, beginning now.</description><identifier>ISSN: 1590-1874</identifier><identifier>EISSN: 1590-3478</identifier><identifier>DOI: 10.1007/s10072-019-3714-1</identifier><identifier>PMID: 30666474</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Alzheimer's disease ; Amyloid ; Blood pressure ; Cerebrovascular diseases ; Cerebrovascular Disorders - enzymology ; Cerebrovascular Disorders - prevention & control ; Cognitive ability ; Dementia ; Dementia - epidemiology ; Dementia - prevention & control ; Dementia disorders ; Etiology ; Fibrillation ; Geriatrics ; Humans ; Medicine ; Medicine & Public Health ; Neurodegenerative diseases ; Neurology ; Neuroradiology ; Neurosciences ; Neurosurgery ; Original Article ; Psychiatry ; Risk factors ; Stroke ; Tau protein</subject><ispartof>Neurological sciences, 2019-04, Vol.40 (4), p.763-767</ispartof><rights>Fondazione Società Italiana di Neurologia 2019</rights><rights>Neurological Sciences is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-176df4446edc538631043c9e78bbbe80f249096c821e57b35b669076cf0aab8a3</citedby><cites>FETCH-LOGICAL-c372t-176df4446edc538631043c9e78bbbe80f249096c821e57b35b669076cf0aab8a3</cites><orcidid>0000-0002-0487-734X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30666474$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hachinski, Vladimir</creatorcontrib><title>Dementia: new vistas and opportunities</title><title>Neurological sciences</title><addtitle>Neurol Sci</addtitle><addtitle>Neurol Sci</addtitle><description>Over the past four decades, Alzheimer disease has become near synonymous with dementia and the amyloid/tau hypothesis as its dominant explanation. However, this monorail approach to etiology has failed to yield a single disease-modifying drug. Part of the explanation stems from the fact that most dementias in the elderly result from interactive Alzheimer and cerebrovascular pathologies. Stroke and dementia share the same risk factors and their control is associated with a decrease in stroke and some dementias. Additionally, intensive control of risk factors and enhancement of protective factors improve cognition. Moreover, anticoagulation of atrial fibrillation patients decreases their chance of developing dementia by 48%. Preliminary data suggest that treating blood pressure to a target of 120 mmHg systolic compared to a target of 140 mmHg decreases the chances of mild cognitive impairment by 19%. The Berlin Manifesto establishes the scientific bases of “preventing dementia by preventing stroke.” Enlarging our vista of dementia to include cerebrovascular disease offers the opportunity of preventing not only stroke, but some dementias, beginning now.</description><subject>Alzheimer's disease</subject><subject>Amyloid</subject><subject>Blood pressure</subject><subject>Cerebrovascular diseases</subject><subject>Cerebrovascular Disorders - enzymology</subject><subject>Cerebrovascular Disorders - prevention & control</subject><subject>Cognitive ability</subject><subject>Dementia</subject><subject>Dementia - epidemiology</subject><subject>Dementia - prevention & control</subject><subject>Dementia disorders</subject><subject>Etiology</subject><subject>Fibrillation</subject><subject>Geriatrics</subject><subject>Humans</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neuroradiology</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Original Article</subject><subject>Psychiatry</subject><subject>Risk factors</subject><subject>Stroke</subject><subject>Tau protein</subject><issn>1590-1874</issn><issn>1590-3478</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp1kMtKxDAUhoMozjj6AG6kIIib6jlNmos7Ga8w4EbXIW1T6TC9mLSKb29KRwXBTRLI9__n8BFyjHCBAOLSj2cSA6qYCmQx7pA5pgpiyoTc3b5RCjYjB96vAQAZ0n0yo8A5Z4LNydmNrW3TV-YqauxH9F753vjINEXUdl3r-qGp-sr6Q7JXmo23R9t7QV7ubp-XD_Hq6f5xeb2KcyqSPkbBi5Ixxm2Rp1RyisBorqyQWZZZCWXCFCieywRtKjKaZpwrEDwvwZhMGrog51Nv59q3wfpe15XP7WZjGtsOXicoFAOaUBrQ0z_ouh1cE7YLFFeYQprKQOFE5a713tlSd66qjfvUCHrUpyeJOkjUo0SNIXOybR6y2hY_iW9rAUgmwIev5tW639H_t34BnJZ5mw</recordid><startdate>20190401</startdate><enddate>20190401</enddate><creator>Hachinski, Vladimir</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0487-734X</orcidid></search><sort><creationdate>20190401</creationdate><title>Dementia: new vistas and opportunities</title><author>Hachinski, Vladimir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-176df4446edc538631043c9e78bbbe80f249096c821e57b35b669076cf0aab8a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Alzheimer's disease</topic><topic>Amyloid</topic><topic>Blood pressure</topic><topic>Cerebrovascular diseases</topic><topic>Cerebrovascular Disorders - 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Academic</collection><jtitle>Neurological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hachinski, Vladimir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dementia: new vistas and opportunities</atitle><jtitle>Neurological sciences</jtitle><stitle>Neurol Sci</stitle><addtitle>Neurol Sci</addtitle><date>2019-04-01</date><risdate>2019</risdate><volume>40</volume><issue>4</issue><spage>763</spage><epage>767</epage><pages>763-767</pages><issn>1590-1874</issn><eissn>1590-3478</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><notes>ObjectType-Review-1</notes><abstract>Over the past four decades, Alzheimer disease has become near synonymous with dementia and the amyloid/tau hypothesis as its dominant explanation. However, this monorail approach to etiology has failed to yield a single disease-modifying drug. Part of the explanation stems from the fact that most dementias in the elderly result from interactive Alzheimer and cerebrovascular pathologies. Stroke and dementia share the same risk factors and their control is associated with a decrease in stroke and some dementias. Additionally, intensive control of risk factors and enhancement of protective factors improve cognition. Moreover, anticoagulation of atrial fibrillation patients decreases their chance of developing dementia by 48%. Preliminary data suggest that treating blood pressure to a target of 120 mmHg systolic compared to a target of 140 mmHg decreases the chances of mild cognitive impairment by 19%. 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subjects | Alzheimer's disease Amyloid Blood pressure Cerebrovascular diseases Cerebrovascular Disorders - enzymology Cerebrovascular Disorders - prevention & control Cognitive ability Dementia Dementia - epidemiology Dementia - prevention & control Dementia disorders Etiology Fibrillation Geriatrics Humans Medicine Medicine & Public Health Neurodegenerative diseases Neurology Neuroradiology Neurosciences Neurosurgery Original Article Psychiatry Risk factors Stroke Tau protein |
title | Dementia: new vistas and opportunities |
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