PI3K/Akt signal pathway involved in the cognitive impairment caused by chronic cerebral hypoperfusion in rats
Chronic cerebral hypoperfusion (CCH) is a common pathophysiological state that usually occurs in conditions such as vascular dementia and Alzheimer's disease, both of which are characterized by cognitive impairment. In previous studies we found that learning capacity and memory were gradually i...
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| Veröffentlicht in: | PloS one 2013-12, Vol.8 (12), p.e81901-e81901 |
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| description | Chronic cerebral hypoperfusion (CCH) is a common pathophysiological state that usually occurs in conditions such as vascular dementia and Alzheimer's disease, both of which are characterized by cognitive impairment. In previous studies we found that learning capacity and memory were gradually impaired with CCH, which altered the expression of synaptophysin, microtubule associated protein-2, growth associated protein-43, brain-derived neurotrophic factor, nerve growth factor, N-methyl-D-aspartate receptor subunit 1, cAMP response element-binding protein and tau hyperphosphorylation in the hippocampus. However, the molecular basis of cognitive impairment in CCH remains obscure. Here we explore the hypothesis that the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signal pathway is involved in this type of cognitive impairment. In order to determine if the expression of PI3K, Akt and phosphorylated Akt (p-Akt) proteins are altered at different stages of CCH with differing levels of cognitive impairment. we performed permanent, bilateral occlusion of the common carotid arteries (2-VO) to induce CCH. Adult male SD rats were randomly divided into sham-operated group, 2-VO 1 week group, 2-VO 4 weeks group and 2-VO 8 weeks group. Behavior tests were utilized to assess cognitive abilities, while western blots were utilized to evaluate protein expression. Rats in the 2-VO groups spent less time exploring novel objects than those in the sham-operated group, and the discrimination ratio of the 2-VO 8 weeks group and the sham-operated group were higher than chance (0.50). Escape latencies in the Morris water maze task in the 2-VO 1 week group were longer than those in the sham-operated group on day 4 and day 5, while escape latencies in the 2-VO 4 weeks group were longer than those in the sham-operated group from day 3 to day 5. Escape latencies in 2-VO 8 weeks group were longer than those in the sham-operated group from day 2 to day 5. NE (northeast) square swimming times in the 2-VO 1 week group, 2-VO 4 weeks group and 2-VO 8 weeks group were shorter than that in the sham-operated group. Western blotting showed that the PI3K expression in the 2-VO 1 week group was lower than that in sham-operated group, while p-Akt expression in the 2-VO 8 weeks group was higher than that in the sham-operated group. There was a linear relationship between the PI3K expression and the discrimination ratio, as well as a linear relationship between the PI3K and NE square swimmin |
| doi_str_mv | 10.1371/journal.pone.0081901 |
| format | Article |
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In previous studies we found that learning capacity and memory were gradually impaired with CCH, which altered the expression of synaptophysin, microtubule associated protein-2, growth associated protein-43, brain-derived neurotrophic factor, nerve growth factor, N-methyl-D-aspartate receptor subunit 1, cAMP response element-binding protein and tau hyperphosphorylation in the hippocampus. However, the molecular basis of cognitive impairment in CCH remains obscure. Here we explore the hypothesis that the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signal pathway is involved in this type of cognitive impairment. In order to determine if the expression of PI3K, Akt and phosphorylated Akt (p-Akt) proteins are altered at different stages of CCH with differing levels of cognitive impairment. we performed permanent, bilateral occlusion of the common carotid arteries (2-VO) to induce CCH. Adult male SD rats were randomly divided into sham-operated group, 2-VO 1 week group, 2-VO 4 weeks group and 2-VO 8 weeks group. Behavior tests were utilized to assess cognitive abilities, while western blots were utilized to evaluate protein expression. Rats in the 2-VO groups spent less time exploring novel objects than those in the sham-operated group, and the discrimination ratio of the 2-VO 8 weeks group and the sham-operated group were higher than chance (0.50). Escape latencies in the Morris water maze task in the 2-VO 1 week group were longer than those in the sham-operated group on day 4 and day 5, while escape latencies in the 2-VO 4 weeks group were longer than those in the sham-operated group from day 3 to day 5. Escape latencies in 2-VO 8 weeks group were longer than those in the sham-operated group from day 2 to day 5. NE (northeast) square swimming times in the 2-VO 1 week group, 2-VO 4 weeks group and 2-VO 8 weeks group were shorter than that in the sham-operated group. Western blotting showed that the PI3K expression in the 2-VO 1 week group was lower than that in sham-operated group, while p-Akt expression in the 2-VO 8 weeks group was higher than that in the sham-operated group. There was a linear relationship between the PI3K expression and the discrimination ratio, as well as a linear relationship between the PI3K and NE square swimming time. Thus, we propose that the PI3K/Akt signal pathway is an important cell pathway that is associated with the cognitive impairment following CCH.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0081901</identifier><identifier>PMID: 24339978</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Alzheimer's disease ; Animal cognition ; Animals ; Arteries ; Aspartate ; Brain ; Brain-derived neurotrophic factor ; Carotid arteries ; Carotid artery ; Cerebral blood flow ; Cerebrovascular Circulation ; Cerebrovascular Disorders - metabolism ; Cerebrovascular Disorders - pathology ; Cerebrovascular Disorders - psychology ; Cognition ; Cognitive ability ; Cyclic AMP response element-binding protein ; Dementia ; Dementia disorders ; Glutamic acid receptors ; Hospitals ; Impairment ; Insulin ; Insulin-like growth factors ; Ischemia ; Kinases ; Laboratory animals ; Learning ; Male ; Maze Learning ; Memory ; N-Methyl-D-aspartic acid receptors ; Nerve growth factor ; Neurodegenerative diseases ; Neurology ; Occlusion ; Pathogenesis ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Protein binding ; Protein kinases ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Sprague-Dawley ; Rodents ; Signal Transduction ; Stroke ; Studies ; Surgery ; Swimming ; Synaptophysin ; Tau protein ; Vascular dementia ; Veins & arteries ; Western blotting</subject><ispartof>PloS one, 2013-12, Vol.8 (12), p.e81901-e81901</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Shu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/3.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Shu et al 2013 Shu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-f0c8b404f4da44378acf27e72e8bb4c6665d1b9b5a4e4cfad5c9b601ca1daaff3</citedby><cites>FETCH-LOGICAL-c758t-f0c8b404f4da44378acf27e72e8bb4c6665d1b9b5a4e4cfad5c9b601ca1daaff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858283/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858283/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24339978$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ma, Daqing</contributor><creatorcontrib>Shu, Yi</creatorcontrib><creatorcontrib>Zhang, Hong</creatorcontrib><creatorcontrib>Kang, Tao</creatorcontrib><creatorcontrib>Zhang, Jun-jian</creatorcontrib><creatorcontrib>Yang, Ying</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><title>PI3K/Akt signal pathway involved in the cognitive impairment caused by chronic cerebral hypoperfusion in rats</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Chronic cerebral hypoperfusion (CCH) is a common pathophysiological state that usually occurs in conditions such as vascular dementia and Alzheimer's disease, both of which are characterized by cognitive impairment. In previous studies we found that learning capacity and memory were gradually impaired with CCH, which altered the expression of synaptophysin, microtubule associated protein-2, growth associated protein-43, brain-derived neurotrophic factor, nerve growth factor, N-methyl-D-aspartate receptor subunit 1, cAMP response element-binding protein and tau hyperphosphorylation in the hippocampus. However, the molecular basis of cognitive impairment in CCH remains obscure. Here we explore the hypothesis that the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signal pathway is involved in this type of cognitive impairment. In order to determine if the expression of PI3K, Akt and phosphorylated Akt (p-Akt) proteins are altered at different stages of CCH with differing levels of cognitive impairment. we performed permanent, bilateral occlusion of the common carotid arteries (2-VO) to induce CCH. Adult male SD rats were randomly divided into sham-operated group, 2-VO 1 week group, 2-VO 4 weeks group and 2-VO 8 weeks group. Behavior tests were utilized to assess cognitive abilities, while western blots were utilized to evaluate protein expression. Rats in the 2-VO groups spent less time exploring novel objects than those in the sham-operated group, and the discrimination ratio of the 2-VO 8 weeks group and the sham-operated group were higher than chance (0.50). Escape latencies in the Morris water maze task in the 2-VO 1 week group were longer than those in the sham-operated group on day 4 and day 5, while escape latencies in the 2-VO 4 weeks group were longer than those in the sham-operated group from day 3 to day 5. Escape latencies in 2-VO 8 weeks group were longer than those in the sham-operated group from day 2 to day 5. NE (northeast) square swimming times in the 2-VO 1 week group, 2-VO 4 weeks group and 2-VO 8 weeks group were shorter than that in the sham-operated group. Western blotting showed that the PI3K expression in the 2-VO 1 week group was lower than that in sham-operated group, while p-Akt expression in the 2-VO 8 weeks group was higher than that in the sham-operated group. There was a linear relationship between the PI3K expression and the discrimination ratio, as well as a linear relationship between the PI3K and NE square swimming time. Thus, we propose that the PI3K/Akt signal pathway is an important cell pathway that is associated with the cognitive impairment following CCH.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Alzheimer's disease</subject><subject>Animal cognition</subject><subject>Animals</subject><subject>Arteries</subject><subject>Aspartate</subject><subject>Brain</subject><subject>Brain-derived neurotrophic factor</subject><subject>Carotid arteries</subject><subject>Carotid artery</subject><subject>Cerebral blood flow</subject><subject>Cerebrovascular Circulation</subject><subject>Cerebrovascular Disorders - metabolism</subject><subject>Cerebrovascular Disorders - pathology</subject><subject>Cerebrovascular Disorders - psychology</subject><subject>Cognition</subject><subject>Cognitive ability</subject><subject>Cyclic AMP response element-binding protein</subject><subject>Dementia</subject><subject>Dementia disorders</subject><subject>Glutamic acid receptors</subject><subject>Hospitals</subject><subject>Impairment</subject><subject>Insulin</subject><subject>Insulin-like growth factors</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Learning</subject><subject>Male</subject><subject>Maze Learning</subject><subject>Memory</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Nerve growth factor</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Occlusion</subject><subject>Pathogenesis</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Protein binding</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Stroke</subject><subject>Studies</subject><subject>Surgery</subject><subject>Swimming</subject><subject>Synaptophysin</subject><subject>Tau protein</subject><subject>Vascular dementia</subject><subject>Veins & arteries</subject><subject>Western blotting</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</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><sourceid>DOA</sourceid><recordid>eNqNk12P1CAYhRujcdfVf2C0iYnRi5mFQgu9MZls_Ji4yRq_bglQaBnb0gU6Ov9eZqe7mZq9MFyU0Occ4PC-SfIcgiVEBJ5v7Oh63i4H26slABSWAD5ITmGJskWRAfTwaH6SPPF-A0COaFE8Tk4yjFBZEnqadF_W6PP56ldIvamjXTrw0Pzmu9T0W9tuVRUnaWhUKm3dm2C2KjXdwI3rVB9SyUcfEbFLZeNsb2QqlVPCRZ9mN9hBOT16Y_u9iePBP00ead569Wz6niU_Prz_fvFpcXn1cX2xulxIktOw0EBSgQHWuOIYI0K51BlRJFNUCCyLosgrKEqRc6yw1LzKZSkKACWHFedao7Pk5cF3aK1nU1KeQRyVOCcERmJ9ICrLN2xwpuNuxyw37GbBuppxF4xsFSviWbQiBCtZYlBlZVlBKqCUuQAFKfZe76bdRtGpSsZkYgIz0_mf3jSstluGaE4ziqLBm8nA2etR-cA646VqW94rO96cu8wgBZRE9NU_6P23m6iaxwuYXtu4r9ybshUmFOE8JyBSy3uoOCrVGRnLSpu4PhO8nQkiE9SfUMcq8Gz97ev_s1c_5-zrI7ZRvA2Nt-0YYun4OYgPoHTWe6f0XcgQsH1X3KbB9l3Bpq6IshfHD3Qnum0D9BeqVglh</recordid><startdate>20131210</startdate><enddate>20131210</enddate><creator>Shu, Yi</creator><creator>Zhang, Hong</creator><creator>Kang, Tao</creator><creator>Zhang, Jun-jian</creator><creator>Yang, Ying</creator><creator>Liu, Hui</creator><creator>Zhang, Lei</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131210</creationdate><title>PI3K/Akt signal pathway involved in the cognitive impairment caused by chronic cerebral hypoperfusion in rats</title><author>Shu, Yi ; Zhang, Hong ; Kang, Tao ; Zhang, Jun-jian ; Yang, Ying ; Liu, Hui ; Zhang, Lei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-f0c8b404f4da44378acf27e72e8bb4c6665d1b9b5a4e4cfad5c9b601ca1daaff3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Alzheimer's disease</topic><topic>Animal cognition</topic><topic>Animals</topic><topic>Arteries</topic><topic>Aspartate</topic><topic>Brain</topic><topic>Brain-derived neurotrophic factor</topic><topic>Carotid arteries</topic><topic>Carotid artery</topic><topic>Cerebral blood flow</topic><topic>Cerebrovascular Circulation</topic><topic>Cerebrovascular Disorders - metabolism</topic><topic>Cerebrovascular Disorders - pathology</topic><topic>Cerebrovascular Disorders - psychology</topic><topic>Cognition</topic><topic>Cognitive ability</topic><topic>Cyclic AMP response element-binding protein</topic><topic>Dementia</topic><topic>Dementia disorders</topic><topic>Glutamic acid receptors</topic><topic>Hospitals</topic><topic>Impairment</topic><topic>Insulin</topic><topic>Insulin-like growth factors</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Learning</topic><topic>Male</topic><topic>Maze Learning</topic><topic>Memory</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Nerve growth factor</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Occlusion</topic><topic>Pathogenesis</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Protein binding</topic><topic>Protein kinases</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shu, Yi</au><au>Zhang, Hong</au><au>Kang, Tao</au><au>Zhang, Jun-jian</au><au>Yang, Ying</au><au>Liu, Hui</au><au>Zhang, Lei</au><au>Ma, Daqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PI3K/Akt signal pathway involved in the cognitive impairment caused by chronic cerebral hypoperfusion in rats</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-12-10</date><risdate>2013</risdate><volume>8</volume><issue>12</issue><spage>e81901</spage><epage>e81901</epage><pages>e81901-e81901</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Chronic cerebral hypoperfusion (CCH) is a common pathophysiological state that usually occurs in conditions such as vascular dementia and Alzheimer's disease, both of which are characterized by cognitive impairment. In previous studies we found that learning capacity and memory were gradually impaired with CCH, which altered the expression of synaptophysin, microtubule associated protein-2, growth associated protein-43, brain-derived neurotrophic factor, nerve growth factor, N-methyl-D-aspartate receptor subunit 1, cAMP response element-binding protein and tau hyperphosphorylation in the hippocampus. However, the molecular basis of cognitive impairment in CCH remains obscure. Here we explore the hypothesis that the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signal pathway is involved in this type of cognitive impairment. In order to determine if the expression of PI3K, Akt and phosphorylated Akt (p-Akt) proteins are altered at different stages of CCH with differing levels of cognitive impairment. we performed permanent, bilateral occlusion of the common carotid arteries (2-VO) to induce CCH. Adult male SD rats were randomly divided into sham-operated group, 2-VO 1 week group, 2-VO 4 weeks group and 2-VO 8 weeks group. Behavior tests were utilized to assess cognitive abilities, while western blots were utilized to evaluate protein expression. Rats in the 2-VO groups spent less time exploring novel objects than those in the sham-operated group, and the discrimination ratio of the 2-VO 8 weeks group and the sham-operated group were higher than chance (0.50). Escape latencies in the Morris water maze task in the 2-VO 1 week group were longer than those in the sham-operated group on day 4 and day 5, while escape latencies in the 2-VO 4 weeks group were longer than those in the sham-operated group from day 3 to day 5. Escape latencies in 2-VO 8 weeks group were longer than those in the sham-operated group from day 2 to day 5. NE (northeast) square swimming times in the 2-VO 1 week group, 2-VO 4 weeks group and 2-VO 8 weeks group were shorter than that in the sham-operated group. Western blotting showed that the PI3K expression in the 2-VO 1 week group was lower than that in sham-operated group, while p-Akt expression in the 2-VO 8 weeks group was higher than that in the sham-operated group. There was a linear relationship between the PI3K expression and the discrimination ratio, as well as a linear relationship between the PI3K and NE square swimming time. Thus, we propose that the PI3K/Akt signal pathway is an important cell pathway that is associated with the cognitive impairment following CCH.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24339978</pmid><doi>10.1371/journal.pone.0081901</doi><tpages>e81901</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-12, Vol.8 (12), p.e81901-e81901 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1466545771 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Alzheimer's disease Animal cognition Animals Arteries Aspartate Brain Brain-derived neurotrophic factor Carotid arteries Carotid artery Cerebral blood flow Cerebrovascular Circulation Cerebrovascular Disorders - metabolism Cerebrovascular Disorders - pathology Cerebrovascular Disorders - psychology Cognition Cognitive ability Cyclic AMP response element-binding protein Dementia Dementia disorders Glutamic acid receptors Hospitals Impairment Insulin Insulin-like growth factors Ischemia Kinases Laboratory animals Learning Male Maze Learning Memory N-Methyl-D-aspartic acid receptors Nerve growth factor Neurodegenerative diseases Neurology Occlusion Pathogenesis Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Protein binding Protein kinases Proteins Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Sprague-Dawley Rodents Signal Transduction Stroke Studies Surgery Swimming Synaptophysin Tau protein Vascular dementia Veins & arteries Western blotting |
| title | PI3K/Akt signal pathway involved in the cognitive impairment caused by chronic cerebral hypoperfusion in rats |
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