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Attentional function and basal forebrain cholinergic neuron morphology during aging in the Ts65Dn mouse model of Down syndrome
Individuals with Down syndrome (DS) exhibit intellectual disability and develop Alzheimer’s disease-like neuropathology during the third decade of life. The Ts65Dn mouse model of DS exhibits key features of both disorders, including impairments in learning, attention and memory, as well as atrophy o...
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Published in: | Brain Structure and Function 2016-12, Vol.221 (9), p.4337-4352 |
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description | Individuals with Down syndrome (DS) exhibit intellectual disability and develop Alzheimer’s disease-like neuropathology during the third decade of life. The Ts65Dn mouse model of DS exhibits key features of both disorders, including impairments in learning, attention and memory, as well as atrophy of basal forebrain cholinergic neurons (BFCNs). The present study evaluated attentional function in relation to BFCN morphology in young (3 months) and middle-aged (12 months) Ts65Dn mice and disomic (2N) controls. Ts65Dn mice exhibited attentional dysfunction at both ages, with greater impairment in older trisomics. Density of BFCNs was significantly lower for Ts65Dn mice independent of age, which may contribute to attentional dysfunction since BFCN density was positively associated with performance on an attention task. BFCN volume decreased with age in 2N but not Ts65Dn mice. Paradoxically, BFCN volume was greater in older trisomic mice, suggestive of a compensatory response. In sum, attentional dysfunction occurred in both young and middle-aged Ts65Dn mice, which may in part reflect reduced density and/or phenotypic alterations in BFCNs. |
doi_str_mv | 10.1007/s00429-015-1164-y |
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The Ts65Dn mouse model of DS exhibits key features of both disorders, including impairments in learning, attention and memory, as well as atrophy of basal forebrain cholinergic neurons (BFCNs). The present study evaluated attentional function in relation to BFCN morphology in young (3 months) and middle-aged (12 months) Ts65Dn mice and disomic (2N) controls. Ts65Dn mice exhibited attentional dysfunction at both ages, with greater impairment in older trisomics. Density of BFCNs was significantly lower for Ts65Dn mice independent of age, which may contribute to attentional dysfunction since BFCN density was positively associated with performance on an attention task. BFCN volume decreased with age in 2N but not Ts65Dn mice. Paradoxically, BFCN volume was greater in older trisomic mice, suggestive of a compensatory response. In sum, attentional dysfunction occurred in both young and middle-aged Ts65Dn mice, which may in part reflect reduced density and/or phenotypic alterations in BFCNs.</description><identifier>ISSN: 1863-2653</identifier><identifier>EISSN: 1863-2661</identifier><identifier>EISSN: 0340-2061</identifier><identifier>DOI: 10.1007/s00429-015-1164-y</identifier><identifier>PMID: 26719290</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Aging ; Animals ; Attention - physiology ; Basal Forebrain - metabolism ; Basal Forebrain - pathology ; Basal Forebrain - physiopathology ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Choline O-Acetyltransferase - metabolism ; Cholinergic Neurons - metabolism ; Cholinergic Neurons - pathology ; Cholinergic Neurons - physiology ; Disease Models, Animal ; Down syndrome ; Down Syndrome - pathology ; Down Syndrome - physiopathology ; Down Syndrome - psychology ; Male ; Mice ; Mice, Transgenic ; Neurology ; Neurons ; Neurosciences ; Original Article</subject><ispartof>Brain Structure and Function, 2016-12, Vol.221 (9), p.4337-4352</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-10cb4cf878069e1ed2771ffcdac60c3de338c019658100028a4c8c9995cd32e53</citedby><cites>FETCH-LOGICAL-c503t-10cb4cf878069e1ed2771ffcdac60c3de338c019658100028a4c8c9995cd32e53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26719290$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Powers, Brian E.</creatorcontrib><creatorcontrib>Velazquez, Ramon</creatorcontrib><creatorcontrib>Kelley, Christy M.</creatorcontrib><creatorcontrib>Ash, Jessica A.</creatorcontrib><creatorcontrib>Strawderman, Myla S.</creatorcontrib><creatorcontrib>Alldred, Melissa J.</creatorcontrib><creatorcontrib>Ginsberg, Stephen D.</creatorcontrib><creatorcontrib>Mufson, Elliott J.</creatorcontrib><creatorcontrib>Strupp, Barbara J.</creatorcontrib><title>Attentional function and basal forebrain cholinergic neuron morphology during aging in the Ts65Dn mouse model of Down syndrome</title><title>Brain Structure and Function</title><addtitle>Brain Struct Funct</addtitle><addtitle>Brain Struct Funct</addtitle><description>Individuals with Down syndrome (DS) exhibit intellectual disability and develop Alzheimer’s disease-like neuropathology during the third decade of life. The Ts65Dn mouse model of DS exhibits key features of both disorders, including impairments in learning, attention and memory, as well as atrophy of basal forebrain cholinergic neurons (BFCNs). The present study evaluated attentional function in relation to BFCN morphology in young (3 months) and middle-aged (12 months) Ts65Dn mice and disomic (2N) controls. Ts65Dn mice exhibited attentional dysfunction at both ages, with greater impairment in older trisomics. Density of BFCNs was significantly lower for Ts65Dn mice independent of age, which may contribute to attentional dysfunction since BFCN density was positively associated with performance on an attention task. BFCN volume decreased with age in 2N but not Ts65Dn mice. Paradoxically, BFCN volume was greater in older trisomic mice, suggestive of a compensatory response. In sum, attentional dysfunction occurred in both young and middle-aged Ts65Dn mice, which may in part reflect reduced density and/or phenotypic alterations in BFCNs.</description><subject>Aging</subject><subject>Animals</subject><subject>Attention - physiology</subject><subject>Basal Forebrain - metabolism</subject><subject>Basal Forebrain - pathology</subject><subject>Basal Forebrain - physiopathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Choline O-Acetyltransferase - metabolism</subject><subject>Cholinergic Neurons - metabolism</subject><subject>Cholinergic Neurons - pathology</subject><subject>Cholinergic Neurons - physiology</subject><subject>Disease Models, Animal</subject><subject>Down syndrome</subject><subject>Down Syndrome - pathology</subject><subject>Down Syndrome - physiopathology</subject><subject>Down Syndrome - psychology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Original Article</subject><issn>1863-2653</issn><issn>1863-2661</issn><issn>0340-2061</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqNkk1r3DAQhk1paNK0P6CXIuglF7cayZalSyEk_YJALslZaOWx18GWtpKd4kt_eyQ2WdJCoZeRGD3zjuajKN4B_QiUNp8ipRVTJYW6BBBVub4oTkAKXjIh4OXhXvPj4nWMd5TWSoJ6VRwz0YBiip4Uv8_nGd08eGdG0i3O5isxriUbE7PLB9wEMzhit34cHIZ-sMThEhI2-bBLXt-vpF3C4Hpi-mwTPW-R3ERRX2ZqiZhsiyPxHbn0vxyJq2uDn_BNcdSZMeLbx_O0uP365ebie3l1_e3HxflVaWvK5xKo3VS2k42kQiFgy5oGus62xgpqeYucS0tBiVqmxlAmTWWlVUrVtuUMa35afN7r7pbNhK1NJQcz6l0YJhNW7c2g_3xxw1b3_l5XuU1VkwTOHgWC_7lgnPU0RIvjaBym-jTISlQMBGX_gabxcAUgE_rhL_TOLyGNIlO8qbniIueGPWWDjzFgd_g3UJ0XQe8XQadF0HkR9Jpi3j8v-BDxNPkEsD0Qd3lyGJ6l_qfqA8pNwIE</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Powers, Brian E.</creator><creator>Velazquez, Ramon</creator><creator>Kelley, Christy M.</creator><creator>Ash, Jessica A.</creator><creator>Strawderman, Myla S.</creator><creator>Alldred, Melissa J.</creator><creator>Ginsberg, Stephen D.</creator><creator>Mufson, Elliott J.</creator><creator>Strupp, Barbara J.</creator><general>Springer Berlin Heidelberg</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>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>8AO</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>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>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161201</creationdate><title>Attentional function and basal forebrain cholinergic neuron morphology during aging in the Ts65Dn mouse model of Down syndrome</title><author>Powers, Brian E. ; Velazquez, Ramon ; Kelley, Christy M. ; Ash, Jessica A. ; Strawderman, Myla S. ; Alldred, Melissa J. ; Ginsberg, Stephen D. ; Mufson, Elliott J. ; Strupp, Barbara J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-10cb4cf878069e1ed2771ffcdac60c3de338c019658100028a4c8c9995cd32e53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aging</topic><topic>Animals</topic><topic>Attention - physiology</topic><topic>Basal Forebrain - metabolism</topic><topic>Basal Forebrain - pathology</topic><topic>Basal Forebrain - physiopathology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Choline O-Acetyltransferase - metabolism</topic><topic>Cholinergic Neurons - metabolism</topic><topic>Cholinergic Neurons - pathology</topic><topic>Cholinergic Neurons - physiology</topic><topic>Disease Models, Animal</topic><topic>Down syndrome</topic><topic>Down Syndrome - pathology</topic><topic>Down Syndrome - physiopathology</topic><topic>Down Syndrome - psychology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurosciences</topic><topic>Original Article</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Powers, Brian E.</creatorcontrib><creatorcontrib>Velazquez, Ramon</creatorcontrib><creatorcontrib>Kelley, Christy M.</creatorcontrib><creatorcontrib>Ash, Jessica A.</creatorcontrib><creatorcontrib>Strawderman, Myla S.</creatorcontrib><creatorcontrib>Alldred, Melissa J.</creatorcontrib><creatorcontrib>Ginsberg, Stephen D.</creatorcontrib><creatorcontrib>Mufson, Elliott J.</creatorcontrib><creatorcontrib>Strupp, Barbara J.</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>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</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 (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>ProQuest Psychology</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Brain Structure and Function</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Powers, Brian E.</au><au>Velazquez, Ramon</au><au>Kelley, Christy M.</au><au>Ash, Jessica A.</au><au>Strawderman, Myla S.</au><au>Alldred, Melissa J.</au><au>Ginsberg, Stephen D.</au><au>Mufson, Elliott J.</au><au>Strupp, Barbara J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Attentional function and basal forebrain cholinergic neuron morphology during aging in the Ts65Dn mouse model of Down syndrome</atitle><jtitle>Brain Structure and Function</jtitle><stitle>Brain Struct Funct</stitle><addtitle>Brain Struct Funct</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>221</volume><issue>9</issue><spage>4337</spage><epage>4352</epage><pages>4337-4352</pages><issn>1863-2653</issn><eissn>1863-2661</eissn><eissn>0340-2061</eissn><abstract>Individuals with Down syndrome (DS) exhibit intellectual disability and develop Alzheimer’s disease-like neuropathology during the third decade of life. The Ts65Dn mouse model of DS exhibits key features of both disorders, including impairments in learning, attention and memory, as well as atrophy of basal forebrain cholinergic neurons (BFCNs). The present study evaluated attentional function in relation to BFCN morphology in young (3 months) and middle-aged (12 months) Ts65Dn mice and disomic (2N) controls. Ts65Dn mice exhibited attentional dysfunction at both ages, with greater impairment in older trisomics. Density of BFCNs was significantly lower for Ts65Dn mice independent of age, which may contribute to attentional dysfunction since BFCN density was positively associated with performance on an attention task. BFCN volume decreased with age in 2N but not Ts65Dn mice. Paradoxically, BFCN volume was greater in older trisomic mice, suggestive of a compensatory response. In sum, attentional dysfunction occurred in both young and middle-aged Ts65Dn mice, which may in part reflect reduced density and/or phenotypic alterations in BFCNs.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26719290</pmid><doi>10.1007/s00429-015-1164-y</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aging Animals Attention - physiology Basal Forebrain - metabolism Basal Forebrain - pathology Basal Forebrain - physiopathology Biomedical and Life Sciences Biomedicine Cell Biology Choline O-Acetyltransferase - metabolism Cholinergic Neurons - metabolism Cholinergic Neurons - pathology Cholinergic Neurons - physiology Disease Models, Animal Down syndrome Down Syndrome - pathology Down Syndrome - physiopathology Down Syndrome - psychology Male Mice Mice, Transgenic Neurology Neurons Neurosciences Original Article |
title | Attentional function and basal forebrain cholinergic neuron morphology during aging in the Ts65Dn mouse model of Down syndrome |
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