Neuroinflammation as a Common Mechanism Associated with the Modifiable Risk Factors for Alzheimer's and Parkinson`s Diseases.
Identifieur interne : 000049 ( PubMed/Checkpoint ); précédent : 000048; suivant : 000050Neuroinflammation as a Common Mechanism Associated with the Modifiable Risk Factors for Alzheimer's and Parkinson`s Diseases.
Auteurs : Jordan Alexander Mckenzie ; Lindsay J. Spielman ; Caitlin B. Pointer ; Jessica R. Lowry ; Ekta Bajwa ; Carolyn W. Lee ; Andis KlegerisSource :
- Current aging science [ 1874-6128 ] ; 2017.
Abstract
Alzheimer's disease (AD) and Parkinson's disease (PD) are among the most common causes of dementia, which increasingly contribute to morbidity and mortality worldwide. A common hallmark in the pathogenesis of these two diseases is neuroinflammation, which is initially triggered by the presence of pathological structures associated with these disorders. Chronic neuroinflammation is sustained by persistent and aberrant microglial activation in the brain, which results in damage and death of neighboring cells, including neurons and glial cells. Two types of risk factors contribute to the development of AD and PD: non-modifiable risk factors and modifiable risk factors. Non-modifiable risk factors include genetic susceptibility that increases an individual's risk of developing the disease, whereas modifiable risk factors include a wide variety of health- and lifestyle-related factors that may be altered by changing individual behaviors. Exposure to environmental toxins could be viewed as a partially modifiable risk factor. This review focuses on four modifiable risk factors including physical inactivity, vascular disease-related conditions, obesity and type two diabetes mellitus, all of which have been identified as risk factors for the development of AD and PD. We highlight that control of the modifiable risk factors is a valid approach for managing the increased incidence of AD and PD. We describe neuroinflammatory mechanisms, which are common to AD and PD, that may link both these neurodegenerative diseases with the four common modifiable risk factors. Understanding these mechanisms could help identify novel therapeutic targets for combating these neurodegenerative diseases.
DOI: 10.2174/1874609810666170315113244
PubMed: 28302047
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Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</nlm:affiliation><wicri:noCountry code="subField">British Columbia</wicri:noCountry></affiliation></author><author><name sortKey="Spielman, Lindsay J" sort="Spielman, Lindsay J" uniqKey="Spielman L" first="Lindsay J" last="Spielman">Lindsay J. Spielman</name><affiliation><nlm:affiliation>The University of British Columbia Okanagan - The Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</nlm:affiliation><wicri:noCountry code="subField">British Columbia</wicri:noCountry></affiliation></author><author><name sortKey="Pointer, Caitlin B" sort="Pointer, Caitlin B" uniqKey="Pointer C" first="Caitlin B" last="Pointer">Caitlin B. Pointer</name><affiliation><nlm:affiliation>The University of British Columbia - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</nlm:affiliation><wicri:noCountry code="subField">British Columbia</wicri:noCountry></affiliation></author><author><name sortKey="Lowry, Jessica R" sort="Lowry, Jessica R" uniqKey="Lowry J" first="Jessica R" last="Lowry">Jessica R. Lowry</name><affiliation><nlm:affiliation>The University of British Columbia Okanagan - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</nlm:affiliation><wicri:noCountry code="subField">British Columbia</wicri:noCountry></affiliation></author><author><name sortKey="Bajwa, Ekta" sort="Bajwa, Ekta" uniqKey="Bajwa E" first="Ekta" last="Bajwa">Ekta Bajwa</name><affiliation><nlm:affiliation>The University of British Columbia Okanagan - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</nlm:affiliation><wicri:noCountry code="subField">British Columbia</wicri:noCountry></affiliation></author><author><name sortKey="Lee, Carolyn W" sort="Lee, Carolyn W" uniqKey="Lee C" first="Carolyn W" last="Lee">Carolyn W. Lee</name><affiliation><nlm:affiliation>The University of British Columbia Okanagan - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</nlm:affiliation><wicri:noCountry code="subField">British Columbia</wicri:noCountry></affiliation></author><author><name sortKey="Klegeris, Andis" sort="Klegeris, Andis" uniqKey="Klegeris A" first="Andis" last="Klegeris">Andis Klegeris</name><affiliation><nlm:affiliation>The University of British Columbia Okanagan - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</nlm:affiliation><wicri:noCountry code="subField">British Columbia</wicri:noCountry></affiliation></author></analytic><series><title level="j">Current aging science</title><idno type="eISSN">1874-6128</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alzheimer's disease (AD) and Parkinson's disease (PD) are among the most common causes of dementia, which increasingly contribute to morbidity and mortality worldwide. A common hallmark in the pathogenesis of these two diseases is neuroinflammation, which is initially triggered by the presence of pathological structures associated with these disorders. Chronic neuroinflammation is sustained by persistent and aberrant microglial activation in the brain, which results in damage and death of neighboring cells, including neurons and glial cells. Two types of risk factors contribute to the development of AD and PD: non-modifiable risk factors and modifiable risk factors. Non-modifiable risk factors include genetic susceptibility that increases an individual's risk of developing the disease, whereas modifiable risk factors include a wide variety of health- and lifestyle-related factors that may be altered by changing individual behaviors. Exposure to environmental toxins could be viewed as a partially modifiable risk factor. This review focuses on four modifiable risk factors including physical inactivity, vascular disease-related conditions, obesity and type two diabetes mellitus, all of which have been identified as risk factors for the development of AD and PD. We highlight that control of the modifiable risk factors is a valid approach for managing the increased incidence of AD and PD. We describe neuroinflammatory mechanisms, which are common to AD and PD, that may link both these neurodegenerative diseases with the four common modifiable risk factors. Understanding these mechanisms could help identify novel therapeutic targets for combating these neurodegenerative diseases.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">28302047</PMID><DateCreated><Year>2017</Year><Month>03</Month><Day>17</Day></DateCreated><DateRevised><Year>2017</Year><Month>03</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1874-6128</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2017</Year><Month>Mar</Month><Day>15</Day></PubDate></JournalIssue><Title>Current aging science</Title><ISOAbbreviation>Curr Aging Sci</ISOAbbreviation></Journal><ArticleTitle>Neuroinflammation as a Common Mechanism Associated with the Modifiable Risk Factors for Alzheimer's and Parkinson`s Diseases.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.2174/1874609810666170315113244</ELocationID><Abstract><AbstractText>Alzheimer's disease (AD) and Parkinson's disease (PD) are among the most common causes of dementia, which increasingly contribute to morbidity and mortality worldwide. A common hallmark in the pathogenesis of these two diseases is neuroinflammation, which is initially triggered by the presence of pathological structures associated with these disorders. Chronic neuroinflammation is sustained by persistent and aberrant microglial activation in the brain, which results in damage and death of neighboring cells, including neurons and glial cells. Two types of risk factors contribute to the development of AD and PD: non-modifiable risk factors and modifiable risk factors. Non-modifiable risk factors include genetic susceptibility that increases an individual's risk of developing the disease, whereas modifiable risk factors include a wide variety of health- and lifestyle-related factors that may be altered by changing individual behaviors. Exposure to environmental toxins could be viewed as a partially modifiable risk factor. This review focuses on four modifiable risk factors including physical inactivity, vascular disease-related conditions, obesity and type two diabetes mellitus, all of which have been identified as risk factors for the development of AD and PD. We highlight that control of the modifiable risk factors is a valid approach for managing the increased incidence of AD and PD. We describe neuroinflammatory mechanisms, which are common to AD and PD, that may link both these neurodegenerative diseases with the four common modifiable risk factors. Understanding these mechanisms could help identify novel therapeutic targets for combating these neurodegenerative diseases.</AbstractText><CopyrightInformation>Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McKenzie</LastName><ForeName>Jordan Alexander</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>University of British Columbia Okanagan - The Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Spielman</LastName><ForeName>Lindsay J</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>The University of British Columbia Okanagan - The Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pointer</LastName><ForeName>Caitlin B</ForeName><Initials>CB</Initials><AffiliationInfo><Affiliation>The University of British Columbia - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lowry</LastName><ForeName>Jessica R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>The University of British Columbia Okanagan - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bajwa</LastName><ForeName>Ekta</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>The University of British Columbia Okanagan - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Carolyn W</ForeName><Initials>CW</Initials><AffiliationInfo><Affiliation>The University of British Columbia Okanagan - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Klegeris</LastName><ForeName>Andis</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>The University of British Columbia Okanagan - Irving K. Barber School of Arts and Sciences Kelowna, British Columbia. Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>03</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United Arab Emirates</Country><MedlineTA>Curr Aging Sci</MedlineTA><NlmUniqueID>101473576</NlmUniqueID><ISSNLinking>1874-6098</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Physical inactivity</Keyword><Keyword MajorTopicYN="N">dementia</Keyword><Keyword MajorTopicYN="N">hypertension</Keyword><Keyword MajorTopicYN="N">microglia</Keyword><Keyword MajorTopicYN="N">obesity</Keyword><Keyword MajorTopicYN="N">type 2 diabetes mellitus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>10</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>03</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>03</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>3</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>3</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>3</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28302047</ArticleId><ArticleId IdType="pii">CAS-EPUB-82288</ArticleId><ArticleId IdType="doi">10.2174/1874609810666170315113244</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Bajwa, Ekta" sort="Bajwa, Ekta" uniqKey="Bajwa E" first="Ekta" last="Bajwa">Ekta Bajwa</name><name sortKey="Klegeris, Andis" sort="Klegeris, Andis" uniqKey="Klegeris A" first="Andis" last="Klegeris">Andis Klegeris</name><name sortKey="Lee, Carolyn W" sort="Lee, Carolyn W" uniqKey="Lee C" first="Carolyn W" last="Lee">Carolyn W. Lee</name><name sortKey="Lowry, Jessica R" sort="Lowry, Jessica R" uniqKey="Lowry J" first="Jessica R" last="Lowry">Jessica R. Lowry</name><name sortKey="Mckenzie, Jordan Alexander" sort="Mckenzie, Jordan Alexander" uniqKey="Mckenzie J" first="Jordan Alexander" last="Mckenzie">Jordan Alexander Mckenzie</name><name sortKey="Pointer, Caitlin B" sort="Pointer, Caitlin B" uniqKey="Pointer C" first="Caitlin B" last="Pointer">Caitlin B. Pointer</name><name sortKey="Spielman, Lindsay J" sort="Spielman, Lindsay J" uniqKey="Spielman L" first="Lindsay J" last="Spielman">Lindsay J. Spielman</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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