Therapies for Prevention and Treatment of Alzheimer’s Disease
Alzheimer’s disease (AD) is the most common cause of dementia associated with a progressive neurodegenerative disorder, with a prevalence of 44 million people throughout the world in 2015, and this figure is estimated to double by 2050. This disease is characterized by blood-brain barrier disruption...
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description | Alzheimer’s disease (AD) is the most common cause of dementia associated with a progressive neurodegenerative disorder, with a prevalence of 44 million people throughout the world in 2015, and this figure is estimated to double by 2050. This disease is characterized by blood-brain barrier disruption, oxidative stress, mitochondrial impairment, neuroinflammation, and hypometabolism; it is related to amyloid-β peptide accumulation and tau hyperphosphorylation as well as a decrease in acetylcholine levels and a reduction of cerebral blood flow. Obesity is a major risk factor for AD, because it induces adipokine dysregulation, which consists of the release of the proinflammatory adipokines and decreased anti-inflammatory adipokines, among other processes. The pharmacological treatments for AD can be divided into two categories: symptomatic treatments such as acetylcholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists and etiology-based treatments such as secretase inhibitors, amyloid binders, and tau therapies. Strategies for prevention of AD through nonpharmacological treatments are associated with lifestyle interventions such as exercise, mental challenges, and socialization as well as caloric restriction and a healthy diet. AD is an important health issue on which all people should be informed so that prevention strategies that minimize the risk of its development may be implemented. |
doi_str_mv | 10.1155/2016/2589276 |
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This disease is characterized by blood-brain barrier disruption, oxidative stress, mitochondrial impairment, neuroinflammation, and hypometabolism; it is related to amyloid-β peptide accumulation and tau hyperphosphorylation as well as a decrease in acetylcholine levels and a reduction of cerebral blood flow. Obesity is a major risk factor for AD, because it induces adipokine dysregulation, which consists of the release of the proinflammatory adipokines and decreased anti-inflammatory adipokines, among other processes. The pharmacological treatments for AD can be divided into two categories: symptomatic treatments such as acetylcholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists and etiology-based treatments such as secretase inhibitors, amyloid binders, and tau therapies. Strategies for prevention of AD through nonpharmacological treatments are associated with lifestyle interventions such as exercise, mental challenges, and socialization as well as caloric restriction and a healthy diet. AD is an important health issue on which all people should be informed so that prevention strategies that minimize the risk of its development may be implemented.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2016/2589276</identifier><identifier>PMID: 27547756</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Advertising executives ; Alzheimer Disease - epidemiology ; Alzheimer Disease - physiopathology ; Alzheimer Disease - prevention & control ; Alzheimer Disease - therapy ; Alzheimer's disease ; Amino acids ; Animal cognition ; Brain ; Care and treatment ; Chromosomes ; Cytokines ; Dementia ; Development and progression ; Diabetes ; Disease prevention ; Drug therapy ; Enzyme inhibitors ; Family medical history ; Genes ; Humans ; Hypotheses ; Laboratories ; Medical imaging ; Metabolic disorders ; Metabolites ; Neuropathology ; NMR ; Nuclear magnetic resonance ; Obesity ; Older people ; Oxidative stress ; Pathogenesis ; Prevention ; Probiotics ; Proteins ; Review ; Risk Factors ; Type 2 diabetes</subject><ispartof>BioMed research international, 2016-01, Vol.2016 (2016), p.1-17</ispartof><rights>Copyright © 2016 J. Mendiola-Precoma et al.</rights><rights>COPYRIGHT 2016 John Wiley & Sons, Inc.</rights><rights>Copyright © 2016 J. Mendiola-Precoma et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2016 J. Mendiola-Precoma et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c532t-f85edc21ca644c65c7ec9a9829bbb85134326c70508894ddc5bb129214a76c873</citedby><cites>FETCH-LOGICAL-c532t-f85edc21ca644c65c7ec9a9829bbb85134326c70508894ddc5bb129214a76c873</cites><orcidid>0000-0002-7420-0211 ; 0000-0002-4777-6135 ; 0000-0002-7768-344X ; 0000-0001-6266-3457</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4980501/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4980501/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27547756$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zhang, Yiying</contributor><creatorcontrib>Garcia-Alcocer, G.</creatorcontrib><creatorcontrib>Padilla, K.</creatorcontrib><creatorcontrib>Berumen, Laura Cristina</creatorcontrib><creatorcontrib>Mendiola-Precoma, J.</creatorcontrib><title>Therapies for Prevention and Treatment of Alzheimer’s Disease</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Alzheimer’s disease (AD) is the most common cause of dementia associated with a progressive neurodegenerative disorder, with a prevalence of 44 million people throughout the world in 2015, and this figure is estimated to double by 2050. This disease is characterized by blood-brain barrier disruption, oxidative stress, mitochondrial impairment, neuroinflammation, and hypometabolism; it is related to amyloid-β peptide accumulation and tau hyperphosphorylation as well as a decrease in acetylcholine levels and a reduction of cerebral blood flow. Obesity is a major risk factor for AD, because it induces adipokine dysregulation, which consists of the release of the proinflammatory adipokines and decreased anti-inflammatory adipokines, among other processes. The pharmacological treatments for AD can be divided into two categories: symptomatic treatments such as acetylcholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists and etiology-based treatments such as secretase inhibitors, amyloid binders, and tau therapies. Strategies for prevention of AD through nonpharmacological treatments are associated with lifestyle interventions such as exercise, mental challenges, and socialization as well as caloric restriction and a healthy diet. AD is an important health issue on which all people should be informed so that prevention strategies that minimize the risk of its development may be implemented.</description><subject>Advertising executives</subject><subject>Alzheimer Disease - epidemiology</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer Disease - prevention & control</subject><subject>Alzheimer Disease - therapy</subject><subject>Alzheimer's disease</subject><subject>Amino acids</subject><subject>Animal cognition</subject><subject>Brain</subject><subject>Care and treatment</subject><subject>Chromosomes</subject><subject>Cytokines</subject><subject>Dementia</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Disease prevention</subject><subject>Drug therapy</subject><subject>Enzyme inhibitors</subject><subject>Family medical history</subject><subject>Genes</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Laboratories</subject><subject>Medical imaging</subject><subject>Metabolic disorders</subject><subject>Metabolites</subject><subject>Neuropathology</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Obesity</subject><subject>Older people</subject><subject>Oxidative stress</subject><subject>Pathogenesis</subject><subject>Prevention</subject><subject>Probiotics</subject><subject>Proteins</subject><subject>Review</subject><subject>Risk Factors</subject><subject>Type 2 diabetes</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNks9uEzEQhy0EolXbG2e0EhckSOvx-u-FKirQIlWCQzhbXu9s42p3HeykCE68Bq_Hk-BVQiic6ost-9OnmfmZkGdATwGEOGMU5BkT2jAlH5FDVgOfSeDweH-u6wNykvMtLUuDpEY-JQdMCa6UkIfkfLHE5FYBc9XFVH1KeIfjOsSxcmNbLRK69VAuqthV8_77EsOA6dePn7l6GzK6jMfkSef6jCe7_Yh8fv9ucXE1u_54-eFifj3zombrWacFtp6Bd5JzL4VX6I0zmpmmabSAmtdMekUF1drwtvWiaYAZBtwp6bWqj8ibrXe1aYaiKjUl19tVCoNL32x0wf77MoalvYl3lhtdrFAEL3eCFL9sMK_tELLHvncjxk22oMFAGYqUD0FryYTRpqAv_kNv4yaNZRITJbWmoPlf6sb1aMPYxVKin6R2LhhVwKWcKny9pXyKOSfs9t0BtVPadkrb7tIu-PP7E9nDf7ItwKstsAxj676GB-qwMNi5e7RRUL7Rb6KOuYY</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Garcia-Alcocer, G.</creator><creator>Padilla, K.</creator><creator>Berumen, Laura Cristina</creator><creator>Mendiola-Precoma, J.</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7420-0211</orcidid><orcidid>https://orcid.org/0000-0002-4777-6135</orcidid><orcidid>https://orcid.org/0000-0002-7768-344X</orcidid><orcidid>https://orcid.org/0000-0001-6266-3457</orcidid></search><sort><creationdate>20160101</creationdate><title>Therapies for Prevention and Treatment of Alzheimer’s Disease</title><author>Garcia-Alcocer, G. ; Padilla, K. ; Berumen, Laura Cristina ; Mendiola-Precoma, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c532t-f85edc21ca644c65c7ec9a9829bbb85134326c70508894ddc5bb129214a76c873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Advertising executives</topic><topic>Alzheimer Disease - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Garcia-Alcocer, G.</au><au>Padilla, K.</au><au>Berumen, Laura Cristina</au><au>Mendiola-Precoma, J.</au><au>Zhang, Yiying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapies for Prevention and Treatment of Alzheimer’s Disease</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>2016</volume><issue>2016</issue><spage>1</spage><epage>17</epage><pages>1-17</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Alzheimer’s disease (AD) is the most common cause of dementia associated with a progressive neurodegenerative disorder, with a prevalence of 44 million people throughout the world in 2015, and this figure is estimated to double by 2050. This disease is characterized by blood-brain barrier disruption, oxidative stress, mitochondrial impairment, neuroinflammation, and hypometabolism; it is related to amyloid-β peptide accumulation and tau hyperphosphorylation as well as a decrease in acetylcholine levels and a reduction of cerebral blood flow. Obesity is a major risk factor for AD, because it induces adipokine dysregulation, which consists of the release of the proinflammatory adipokines and decreased anti-inflammatory adipokines, among other processes. The pharmacological treatments for AD can be divided into two categories: symptomatic treatments such as acetylcholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists and etiology-based treatments such as secretase inhibitors, amyloid binders, and tau therapies. Strategies for prevention of AD through nonpharmacological treatments are associated with lifestyle interventions such as exercise, mental challenges, and socialization as well as caloric restriction and a healthy diet. AD is an important health issue on which all people should be informed so that prevention strategies that minimize the risk of its development may be implemented.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>27547756</pmid><doi>10.1155/2016/2589276</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-7420-0211</orcidid><orcidid>https://orcid.org/0000-0002-4777-6135</orcidid><orcidid>https://orcid.org/0000-0002-7768-344X</orcidid><orcidid>https://orcid.org/0000-0001-6266-3457</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Advertising executives Alzheimer Disease - epidemiology Alzheimer Disease - physiopathology Alzheimer Disease - prevention & control Alzheimer Disease - therapy Alzheimer's disease Amino acids Animal cognition Brain Care and treatment Chromosomes Cytokines Dementia Development and progression Diabetes Disease prevention Drug therapy Enzyme inhibitors Family medical history Genes Humans Hypotheses Laboratories Medical imaging Metabolic disorders Metabolites Neuropathology NMR Nuclear magnetic resonance Obesity Older people Oxidative stress Pathogenesis Prevention Probiotics Proteins Review Risk Factors Type 2 diabetes |
title | Therapies for Prevention and Treatment of Alzheimer’s Disease |
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