Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model
Vascular pathology and Alzheimer disease (AD) pathology have been shown to coexist in the brains of dementia patients. We investigated how cognitive impairment could be exacerbated in a rat model of combined injury through the interaction of chronic cerebral hypoperfusion and amyloid beta (Aβ) toxic...
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| Veröffentlicht in: | Stroke (1970) 2011-09, Vol.42 (9), p.2595-2604 |
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| creator | CHOI, Bo-Ryoung SANG RIM LEE CHUNG, Chin-Sang LEE, Seong-Ryong HAHN YOUNG KIM HAN, Jung-Soo WOO, Sang-Keun KYEONG MIN KIM CHOI, Dong-Hee KYOUNG JA KWON HAN, Seol-Heui CHAN YOUNG SHIN LEE, Jongmin |
| description | Vascular pathology and Alzheimer disease (AD) pathology have been shown to coexist in the brains of dementia patients. We investigated how cognitive impairment could be exacerbated in a rat model of combined injury through the interaction of chronic cerebral hypoperfusion and amyloid beta (Aβ) toxicity.
In Wistar rats, chronic cerebral hypoperfusion was modeled by permanent occlusion of bilateral common carotid arteries (BCCAo). Further, AD pathology was modeled by bilateral intracerebroventricular Aβ (Aβ toxicity) using a nonphysiological Aβ peptide (Aβ 25 to 35). The experimental animals were divided into 4 groups, including sham, single injury (Aβ toxicity or BCCAo), and combined injury (BCCAo-Aβ toxicity) groups (n=7 per group) . Cerebral blood flow and metabolism were measured using small animal positron emission tomography. A Morris water maze task, novel object location and recognition tests, and histological investigation, including neuronal cell death, apoptosis, neuroinflammation, and AD-related pathology, were performed.
Spatial memory impairment was synergistically exacerbated in the BCCAo-Aβ toxicity group as compared to the BCCAo or Aβ toxicity groups (P |
| doi_str_mv | 10.1161/STROKEAHA.111.620179 |
| format | Article |
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In Wistar rats, chronic cerebral hypoperfusion was modeled by permanent occlusion of bilateral common carotid arteries (BCCAo). Further, AD pathology was modeled by bilateral intracerebroventricular Aβ (Aβ toxicity) using a nonphysiological Aβ peptide (Aβ 25 to 35). The experimental animals were divided into 4 groups, including sham, single injury (Aβ toxicity or BCCAo), and combined injury (BCCAo-Aβ toxicity) groups (n=7 per group) . Cerebral blood flow and metabolism were measured using small animal positron emission tomography. A Morris water maze task, novel object location and recognition tests, and histological investigation, including neuronal cell death, apoptosis, neuroinflammation, and AD-related pathology, were performed.
Spatial memory impairment was synergistically exacerbated in the BCCAo-Aβ toxicity group as compared to the BCCAo or Aβ toxicity groups (P<0.05). Compared to the sham group, neuroinflammation with microglial or astroglial activation was increased both in multiple white matter lesions and the hippocampus in other experimental groups. AD-related pathology was enhanced in the BCCAo-Aβ toxicity group compared to the Aβ toxicity group.
Our experimental results support a clinical hypothesis of the deleterious interaction between chronic cerebral hypoperfusion and Aβ toxicity. Chronic cerebral hypoperfusion-induced perturbation in the equilibrium of AD-related pathology may exacerbate cognitive impairment in a rat model of combined injury.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/STROKEAHA.111.620179</identifier><identifier>PMID: 21737797</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer Disease - physiopathology ; Amyloid beta-Peptides - metabolism ; Animals ; Apoptosis ; Biological and medical sciences ; Cerebrovascular Circulation ; Chronic Disease ; Dementia, Vascular - diagnostic imaging ; Dementia, Vascular - metabolism ; Dementia, Vascular - pathology ; Dementia, Vascular - physiopathology ; Disease Models, Animal ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Male ; Maze Learning ; Medical sciences ; Memory Disorders - diagnostic imaging ; Memory Disorders - metabolism ; Memory Disorders - pathology ; Memory Disorders - physiopathology ; Nervous system (semeiology, syndromes) ; Neurology ; Positron-Emission Tomography ; Radiography ; Rats ; Rats, Wistar ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 2011-09, Vol.42 (9), p.2595-2604</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-e51573eca01b1f8f206e551eeb727a510d7175571ff0ed3f389a6dfcba7602d63</citedby><cites>FETCH-LOGICAL-c433t-e51573eca01b1f8f206e551eeb727a510d7175571ff0ed3f389a6dfcba7602d63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3673,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24504662$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21737797$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHOI, Bo-Ryoung</creatorcontrib><creatorcontrib>SANG RIM LEE</creatorcontrib><creatorcontrib>CHUNG, Chin-Sang</creatorcontrib><creatorcontrib>LEE, Seong-Ryong</creatorcontrib><creatorcontrib>HAHN YOUNG KIM</creatorcontrib><creatorcontrib>HAN, Jung-Soo</creatorcontrib><creatorcontrib>WOO, Sang-Keun</creatorcontrib><creatorcontrib>KYEONG MIN KIM</creatorcontrib><creatorcontrib>CHOI, Dong-Hee</creatorcontrib><creatorcontrib>KYOUNG JA KWON</creatorcontrib><creatorcontrib>HAN, Seol-Heui</creatorcontrib><creatorcontrib>CHAN YOUNG SHIN</creatorcontrib><creatorcontrib>LEE, Jongmin</creatorcontrib><title>Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Vascular pathology and Alzheimer disease (AD) pathology have been shown to coexist in the brains of dementia patients. We investigated how cognitive impairment could be exacerbated in a rat model of combined injury through the interaction of chronic cerebral hypoperfusion and amyloid beta (Aβ) toxicity.
In Wistar rats, chronic cerebral hypoperfusion was modeled by permanent occlusion of bilateral common carotid arteries (BCCAo). Further, AD pathology was modeled by bilateral intracerebroventricular Aβ (Aβ toxicity) using a nonphysiological Aβ peptide (Aβ 25 to 35). The experimental animals were divided into 4 groups, including sham, single injury (Aβ toxicity or BCCAo), and combined injury (BCCAo-Aβ toxicity) groups (n=7 per group) . Cerebral blood flow and metabolism were measured using small animal positron emission tomography. A Morris water maze task, novel object location and recognition tests, and histological investigation, including neuronal cell death, apoptosis, neuroinflammation, and AD-related pathology, were performed.
Spatial memory impairment was synergistically exacerbated in the BCCAo-Aβ toxicity group as compared to the BCCAo or Aβ toxicity groups (P<0.05). Compared to the sham group, neuroinflammation with microglial or astroglial activation was increased both in multiple white matter lesions and the hippocampus in other experimental groups. AD-related pathology was enhanced in the BCCAo-Aβ toxicity group compared to the Aβ toxicity group.
Our experimental results support a clinical hypothesis of the deleterious interaction between chronic cerebral hypoperfusion and Aβ toxicity. Chronic cerebral hypoperfusion-induced perturbation in the equilibrium of AD-related pathology may exacerbate cognitive impairment in a rat model of combined injury.</description><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Cerebrovascular Circulation</subject><subject>Chronic Disease</subject><subject>Dementia, Vascular - diagnostic imaging</subject><subject>Dementia, Vascular - metabolism</subject><subject>Dementia, Vascular - pathology</subject><subject>Dementia, Vascular - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Male</subject><subject>Maze Learning</subject><subject>Medical sciences</subject><subject>Memory Disorders - diagnostic imaging</subject><subject>Memory Disorders - metabolism</subject><subject>Memory Disorders - pathology</subject><subject>Memory Disorders - physiopathology</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Positron-Emission Tomography</subject><subject>Radiography</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFFr2zAUhUVZabJu_6AMvezRna5kSfFjCO0SllJo02cjy1eJhm0ZyYEa-uPnkjZ7uhzOd-7DR8gNsFsABb-ed0-Pf-6W6-UU4VZxBrq4IHOQPM9yxRdfyJwxUWQ8L4oZ-ZrSX8YYFwt5RWYctNC60HPy9jx2GPc-Dd7SB2xDHOmm7Y2PLXYD3R1iOO4PdDgg3XQDRmMHHzoaHF1NVTeNVhixiqah67EPPUZ3TO-E6Wq6bJuxCb6mu_DqrR9G6qeCPpmBPoQam2_k0pkm4fePe01e7u92q3W2ffy9WS23mc2FGDKUILVAaxhU4BaOM4VSAmKluTYSWK1BS6nBOYa1cGJRGFU7WxmtGK-VuCb56a-NIaWIruyjb00cS2Dlu8zyLHOKUJ5kTrMfp1l_rFqsz6NPexPw8wMwyZrGRdNZn_5zuWS5Ulz8A_Iaf-k</recordid><startdate>20110901</startdate><enddate>20110901</enddate><creator>CHOI, Bo-Ryoung</creator><creator>SANG RIM LEE</creator><creator>CHUNG, Chin-Sang</creator><creator>LEE, Seong-Ryong</creator><creator>HAHN YOUNG KIM</creator><creator>HAN, Jung-Soo</creator><creator>WOO, Sang-Keun</creator><creator>KYEONG MIN KIM</creator><creator>CHOI, Dong-Hee</creator><creator>KYOUNG JA KWON</creator><creator>HAN, Seol-Heui</creator><creator>CHAN YOUNG SHIN</creator><creator>LEE, Jongmin</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</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></search><sort><creationdate>20110901</creationdate><title>Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model</title><author>CHOI, Bo-Ryoung ; SANG RIM LEE ; CHUNG, Chin-Sang ; LEE, Seong-Ryong ; HAHN YOUNG KIM ; HAN, Jung-Soo ; WOO, Sang-Keun ; KYEONG MIN KIM ; CHOI, Dong-Hee ; KYOUNG JA KWON ; HAN, Seol-Heui ; CHAN YOUNG SHIN ; LEE, Jongmin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-e51573eca01b1f8f206e551eeb727a510d7175571ff0ed3f389a6dfcba7602d63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Cerebrovascular Circulation</topic><topic>Chronic Disease</topic><topic>Dementia, Vascular - diagnostic imaging</topic><topic>Dementia, Vascular - metabolism</topic><topic>Dementia, Vascular - pathology</topic><topic>Dementia, Vascular - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Male</topic><topic>Maze Learning</topic><topic>Medical sciences</topic><topic>Memory Disorders - diagnostic imaging</topic><topic>Memory Disorders - metabolism</topic><topic>Memory Disorders - pathology</topic><topic>Memory Disorders - physiopathology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Positron-Emission Tomography</topic><topic>Radiography</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHOI, Bo-Ryoung</creatorcontrib><creatorcontrib>SANG RIM LEE</creatorcontrib><creatorcontrib>CHUNG, Chin-Sang</creatorcontrib><creatorcontrib>LEE, Seong-Ryong</creatorcontrib><creatorcontrib>HAHN YOUNG KIM</creatorcontrib><creatorcontrib>HAN, Jung-Soo</creatorcontrib><creatorcontrib>WOO, Sang-Keun</creatorcontrib><creatorcontrib>KYEONG MIN KIM</creatorcontrib><creatorcontrib>CHOI, Dong-Hee</creatorcontrib><creatorcontrib>KYOUNG JA KWON</creatorcontrib><creatorcontrib>HAN, Seol-Heui</creatorcontrib><creatorcontrib>CHAN YOUNG SHIN</creatorcontrib><creatorcontrib>LEE, Jongmin</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHOI, Bo-Ryoung</au><au>SANG RIM LEE</au><au>CHUNG, Chin-Sang</au><au>LEE, Seong-Ryong</au><au>HAHN YOUNG KIM</au><au>HAN, Jung-Soo</au><au>WOO, Sang-Keun</au><au>KYEONG MIN KIM</au><au>CHOI, Dong-Hee</au><au>KYOUNG JA KWON</au><au>HAN, Seol-Heui</au><au>CHAN YOUNG SHIN</au><au>LEE, Jongmin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2011-09-01</date><risdate>2011</risdate><volume>42</volume><issue>9</issue><spage>2595</spage><epage>2604</epage><pages>2595-2604</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Vascular pathology and Alzheimer disease (AD) pathology have been shown to coexist in the brains of dementia patients. We investigated how cognitive impairment could be exacerbated in a rat model of combined injury through the interaction of chronic cerebral hypoperfusion and amyloid beta (Aβ) toxicity.
In Wistar rats, chronic cerebral hypoperfusion was modeled by permanent occlusion of bilateral common carotid arteries (BCCAo). Further, AD pathology was modeled by bilateral intracerebroventricular Aβ (Aβ toxicity) using a nonphysiological Aβ peptide (Aβ 25 to 35). The experimental animals were divided into 4 groups, including sham, single injury (Aβ toxicity or BCCAo), and combined injury (BCCAo-Aβ toxicity) groups (n=7 per group) . Cerebral blood flow and metabolism were measured using small animal positron emission tomography. A Morris water maze task, novel object location and recognition tests, and histological investigation, including neuronal cell death, apoptosis, neuroinflammation, and AD-related pathology, were performed.
Spatial memory impairment was synergistically exacerbated in the BCCAo-Aβ toxicity group as compared to the BCCAo or Aβ toxicity groups (P<0.05). Compared to the sham group, neuroinflammation with microglial or astroglial activation was increased both in multiple white matter lesions and the hippocampus in other experimental groups. AD-related pathology was enhanced in the BCCAo-Aβ toxicity group compared to the Aβ toxicity group.
Our experimental results support a clinical hypothesis of the deleterious interaction between chronic cerebral hypoperfusion and Aβ toxicity. Chronic cerebral hypoperfusion-induced perturbation in the equilibrium of AD-related pathology may exacerbate cognitive impairment in a rat model of combined injury.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>21737797</pmid><doi>10.1161/STROKEAHA.111.620179</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Stroke (1970), 2011-09, Vol.42 (9), p.2595-2604 |
| issn | 0039-2499 1524-4628 |
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| source | MEDLINE; American Heart Association; Journals@Ovid Ovid Autoload; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer Disease - physiopathology Amyloid beta-Peptides - metabolism Animals Apoptosis Biological and medical sciences Cerebrovascular Circulation Chronic Disease Dementia, Vascular - diagnostic imaging Dementia, Vascular - metabolism Dementia, Vascular - pathology Dementia, Vascular - physiopathology Disease Models, Animal Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Male Maze Learning Medical sciences Memory Disorders - diagnostic imaging Memory Disorders - metabolism Memory Disorders - pathology Memory Disorders - physiopathology Nervous system (semeiology, syndromes) Neurology Positron-Emission Tomography Radiography Rats Rats, Wistar Vascular diseases and vascular malformations of the nervous system |
| title | Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model |
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