Network abnormalities and interneuron dysfunction in Alzheimer disease
Key Points The brain controls the function of neural circuits and networks, in part, by modulating the synchrony of their components. Network hypersynchrony and altered oscillatory rhythmic activity may underlie cognitive abnormalities in Alzheimer disease (AD). In AD, network activities that suppor...
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| Veröffentlicht in: | Nature reviews. Neuroscience 2016-12, Vol.17 (12), p.777-792 |
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| creator | Palop, Jorge J. Mucke, Lennart |
| description | Key Points
The brain controls the function of neural circuits and networks, in part, by modulating the synchrony of their components.
Network hypersynchrony and altered oscillatory rhythmic activity may underlie cognitive abnormalities in Alzheimer disease (AD).
In AD, network activities that support cognition are altered decades before clinical disease onset, and the affected networks predict future pathology and brain atrophy.
Although the precise causes and pathophysiological consequences of these network alterations remain to be fully elucidated, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders.
Several lines of evidence suggest that modulating interneuron-dependent network alterations could be a useful therapeutic strategy to improve brain functions in these conditions.
The cognitive abnormalities observed in Alzheimer disease (AD) may be linked to alterations in oscillatory rhythmic activity and neuronal network hypersynchrony. Palop and Mucke review these links and explore how countering these network abnormalities and interneuron dysfunction may hold therapeutic potential for AD.
The function of neural circuits and networks can be controlled, in part, by modulating the synchrony of their components' activities. Network hypersynchrony and altered oscillatory rhythmic activity may contribute to cognitive abnormalities in Alzheimer disease (AD). In this condition, network activities that support cognition are altered decades before clinical disease onset, and these alterations predict future pathology and brain atrophy. Although the precise causes and pathophysiological consequences of these network alterations remain to be defined, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders. Here, we explore the concept that modulating these mechanisms may help to improve brain function in these conditions. |
| doi_str_mv | 10.1038/nrn.2016.141 |
| format | Article |
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The brain controls the function of neural circuits and networks, in part, by modulating the synchrony of their components.
Network hypersynchrony and altered oscillatory rhythmic activity may underlie cognitive abnormalities in Alzheimer disease (AD).
In AD, network activities that support cognition are altered decades before clinical disease onset, and the affected networks predict future pathology and brain atrophy.
Although the precise causes and pathophysiological consequences of these network alterations remain to be fully elucidated, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders.
Several lines of evidence suggest that modulating interneuron-dependent network alterations could be a useful therapeutic strategy to improve brain functions in these conditions.
The cognitive abnormalities observed in Alzheimer disease (AD) may be linked to alterations in oscillatory rhythmic activity and neuronal network hypersynchrony. Palop and Mucke review these links and explore how countering these network abnormalities and interneuron dysfunction may hold therapeutic potential for AD.
The function of neural circuits and networks can be controlled, in part, by modulating the synchrony of their components' activities. Network hypersynchrony and altered oscillatory rhythmic activity may contribute to cognitive abnormalities in Alzheimer disease (AD). In this condition, network activities that support cognition are altered decades before clinical disease onset, and these alterations predict future pathology and brain atrophy. Although the precise causes and pathophysiological consequences of these network alterations remain to be defined, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders. Here, we explore the concept that modulating these mechanisms may help to improve brain function in these conditions.</description><identifier>ISSN: 1471-003X</identifier><identifier>EISSN: 1471-0048</identifier><identifier>EISSN: 1469-3178</identifier><identifier>DOI: 10.1038/nrn.2016.141</identifier><identifier>PMID: 27829687</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>14 ; 59 ; 631/378/1689/1283 ; 631/378/1689/178 ; 631/378/1697 ; Alzheimer Disease - pathology ; Alzheimer Disease - physiopathology ; Alzheimer's disease ; Animal Genetics and Genomics ; Animals ; Behavioral Sciences ; Biological Techniques ; Biomedicine ; Brain ; Brain - pathology ; Brain - physiopathology ; Care and treatment ; Cognition Disorders - pathology ; Cognition Disorders - physiopathology ; Cognitive ability ; Development and progression ; Disease ; Health aspects ; Humans ; Interneurons - pathology ; Interneurons - physiology ; Memory ; Nerve Net - pathology ; Nerve Net - physiopathology ; Neural circuitry ; Neural Pathways - pathology ; Neural Pathways - physiopathology ; Neurobiology ; Neurosciences ; review-article</subject><ispartof>Nature reviews. Neuroscience, 2016-12, Vol.17 (12), p.777-792</ispartof><rights>Springer Nature Limited 2016</rights><rights>COPYRIGHT 2016 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c616t-7f1cc828e77ab4283b9c04225bba768fd5fa73ddfa2ce438af850716b1099ee53</citedby><cites>FETCH-LOGICAL-c616t-7f1cc828e77ab4283b9c04225bba768fd5fa73ddfa2ce438af850716b1099ee53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27829687$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Palop, Jorge J.</creatorcontrib><creatorcontrib>Mucke, Lennart</creatorcontrib><title>Network abnormalities and interneuron dysfunction in Alzheimer disease</title><title>Nature reviews. Neuroscience</title><addtitle>Nat Rev Neurosci</addtitle><addtitle>Nat Rev Neurosci</addtitle><description>Key Points
The brain controls the function of neural circuits and networks, in part, by modulating the synchrony of their components.
Network hypersynchrony and altered oscillatory rhythmic activity may underlie cognitive abnormalities in Alzheimer disease (AD).
In AD, network activities that support cognition are altered decades before clinical disease onset, and the affected networks predict future pathology and brain atrophy.
Although the precise causes and pathophysiological consequences of these network alterations remain to be fully elucidated, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders.
Several lines of evidence suggest that modulating interneuron-dependent network alterations could be a useful therapeutic strategy to improve brain functions in these conditions.
The cognitive abnormalities observed in Alzheimer disease (AD) may be linked to alterations in oscillatory rhythmic activity and neuronal network hypersynchrony. Palop and Mucke review these links and explore how countering these network abnormalities and interneuron dysfunction may hold therapeutic potential for AD.
The function of neural circuits and networks can be controlled, in part, by modulating the synchrony of their components' activities. Network hypersynchrony and altered oscillatory rhythmic activity may contribute to cognitive abnormalities in Alzheimer disease (AD). In this condition, network activities that support cognition are altered decades before clinical disease onset, and these alterations predict future pathology and brain atrophy. Although the precise causes and pathophysiological consequences of these network alterations remain to be defined, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders. Here, we explore the concept that modulating these mechanisms may help to improve brain function in these conditions.</description><subject>14</subject><subject>59</subject><subject>631/378/1689/1283</subject><subject>631/378/1689/178</subject><subject>631/378/1697</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer's disease</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Behavioral Sciences</subject><subject>Biological Techniques</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Brain - pathology</subject><subject>Brain - physiopathology</subject><subject>Care and treatment</subject><subject>Cognition Disorders - pathology</subject><subject>Cognition Disorders - physiopathology</subject><subject>Cognitive ability</subject><subject>Development and progression</subject><subject>Disease</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Interneurons - pathology</subject><subject>Interneurons - physiology</subject><subject>Memory</subject><subject>Nerve Net - pathology</subject><subject>Nerve Net - physiopathology</subject><subject>Neural circuitry</subject><subject>Neural Pathways - pathology</subject><subject>Neural Pathways - physiopathology</subject><subject>Neurobiology</subject><subject>Neurosciences</subject><subject>review-article</subject><issn>1471-003X</issn><issn>1471-0048</issn><issn>1469-3178</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><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>eNqNks1v1DAQxSMEoh9w44wiceFAFo_t2M4FaVXRglTBBSRuluOMty6JXeykqPz1eLVlaVEPyAePPL95Gj-9qnoBZAWEqbchhRUlIFbA4VF1CFxCQwhXj_c1-3ZQHeV8SQoFUjytDqhUtBNKHlann3D-GdP32vQhpsmMfvaYaxOG2ocZU8AlxVAPN9ktwc6-1D7U6_HXBfoJUz34jCbjs-qJM2PG57f3cfX19P2Xkw_N-eezjyfr88YKEHMjHVirqEIpTc-pYn1nCae07XsjhXJD64xkw-AMtciZMk61RILogXQdYsuOq3c73auln3CwGOZkRn2V_GTSjY7G6_ud4C_0Jl5rBYICEUXg9a1Aij8WzLOefLY4jiZgXLIGxQUnlLfdf6CsA6I4IwV99Q96GZcUihNbQeCEM6b-UhszovbBxbKi3YrqNZeEc9G1rFCrB6hyBpy8jQGdL-_3Bt7sBmyKOSd0ezuA6G1EdImI3kZEl4gU_OVdC_fwn0wUoNkBubTCBtOdzzwk-Bsmw8WC</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Palop, Jorge J.</creator><creator>Mucke, Lennart</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161201</creationdate><title>Network abnormalities and interneuron dysfunction in Alzheimer disease</title><author>Palop, Jorge J. ; Mucke, Lennart</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c616t-7f1cc828e77ab4283b9c04225bba768fd5fa73ddfa2ce438af850716b1099ee53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>14</topic><topic>59</topic><topic>631/378/1689/1283</topic><topic>631/378/1689/178</topic><topic>631/378/1697</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer's disease</topic><topic>Animal Genetics and Genomics</topic><topic>Animals</topic><topic>Behavioral Sciences</topic><topic>Biological Techniques</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Brain - pathology</topic><topic>Brain - physiopathology</topic><topic>Care and treatment</topic><topic>Cognition Disorders - pathology</topic><topic>Cognition Disorders - physiopathology</topic><topic>Cognitive ability</topic><topic>Development and progression</topic><topic>Disease</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Interneurons - pathology</topic><topic>Interneurons - physiology</topic><topic>Memory</topic><topic>Nerve Net - pathology</topic><topic>Nerve Net - physiopathology</topic><topic>Neural circuitry</topic><topic>Neural Pathways - pathology</topic><topic>Neural Pathways - physiopathology</topic><topic>Neurobiology</topic><topic>Neurosciences</topic><topic>review-article</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Palop, Jorge J.</creatorcontrib><creatorcontrib>Mucke, Lennart</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature reviews. Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Palop, Jorge J.</au><au>Mucke, Lennart</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Network abnormalities and interneuron dysfunction in Alzheimer disease</atitle><jtitle>Nature reviews. Neuroscience</jtitle><stitle>Nat Rev Neurosci</stitle><addtitle>Nat Rev Neurosci</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>17</volume><issue>12</issue><spage>777</spage><epage>792</epage><pages>777-792</pages><issn>1471-003X</issn><eissn>1471-0048</eissn><eissn>1469-3178</eissn><abstract>Key Points
The brain controls the function of neural circuits and networks, in part, by modulating the synchrony of their components.
Network hypersynchrony and altered oscillatory rhythmic activity may underlie cognitive abnormalities in Alzheimer disease (AD).
In AD, network activities that support cognition are altered decades before clinical disease onset, and the affected networks predict future pathology and brain atrophy.
Although the precise causes and pathophysiological consequences of these network alterations remain to be fully elucidated, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders.
Several lines of evidence suggest that modulating interneuron-dependent network alterations could be a useful therapeutic strategy to improve brain functions in these conditions.
The cognitive abnormalities observed in Alzheimer disease (AD) may be linked to alterations in oscillatory rhythmic activity and neuronal network hypersynchrony. Palop and Mucke review these links and explore how countering these network abnormalities and interneuron dysfunction may hold therapeutic potential for AD.
The function of neural circuits and networks can be controlled, in part, by modulating the synchrony of their components' activities. Network hypersynchrony and altered oscillatory rhythmic activity may contribute to cognitive abnormalities in Alzheimer disease (AD). In this condition, network activities that support cognition are altered decades before clinical disease onset, and these alterations predict future pathology and brain atrophy. Although the precise causes and pathophysiological consequences of these network alterations remain to be defined, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders. Here, we explore the concept that modulating these mechanisms may help to improve brain function in these conditions.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27829687</pmid><doi>10.1038/nrn.2016.141</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 14 59 631/378/1689/1283 631/378/1689/178 631/378/1697 Alzheimer Disease - pathology Alzheimer Disease - physiopathology Alzheimer's disease Animal Genetics and Genomics Animals Behavioral Sciences Biological Techniques Biomedicine Brain Brain - pathology Brain - physiopathology Care and treatment Cognition Disorders - pathology Cognition Disorders - physiopathology Cognitive ability Development and progression Disease Health aspects Humans Interneurons - pathology Interneurons - physiology Memory Nerve Net - pathology Nerve Net - physiopathology Neural circuitry Neural Pathways - pathology Neural Pathways - physiopathology Neurobiology Neurosciences review-article |
| title | Network abnormalities and interneuron dysfunction in Alzheimer disease |
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