Protection against developmental retardation in apolipoprotein E‐deficient mice by a fatty neuropeptide: Implications for early treatment of Alzheimer's disease
Stearyl‐Nle‐17‐VIP (SNV) is a novel agonist of vasoactive intestinal peptide (VIP) exhibiting a 100‐fold greater potency than the parent molecule and specificity for a receptor associated with neuronal survival. Here, mice deficient in apolipoprotein E (ApoE), a molecule associated with the etiology...
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| Veröffentlicht in: | Journal of neurobiology 1997-09, Vol.33 (3), p.329-342 |
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| container_title | Journal of neurobiology |
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| creator | Gozes, Illana Bachar, Michal Bardea, Amos Davidson, Ariane Rubinraut, Sarah Fridkin, Mati Giladi, Eli |
| description | Stearyl‐Nle‐17‐VIP (SNV) is a novel agonist of vasoactive intestinal peptide (VIP) exhibiting a 100‐fold greater potency than the parent molecule and specificity for a receptor associated with neuronal survival. Here, mice deficient in apolipoprotein E (ApoE), a molecule associated with the etiology of Alzheimer's disease, served as a model to investigate the developmental and protective effects of SNV. In comparison to control animals, the deficient mice exhibited (a) reduced amounts of VIP messenger RNA; (b) decreased cholinergic activity (c) significant retardation in the acquisition of developmental milestones: forelimb placing behavior and cliff avoidance behavior; and (d) learning and memory impairments. Daily injections of SNV to ApoE‐deficient newborn pups resulted in increased cholinergic activity and marked improvements in the time of acquisition of behavioral milestones, with peptide‐treated animals developing as fast as control animals and exhibiting improved cognitive functions after cessation of peptide treatment. Specificity was demonstrated in that treatment with a related peptide (PACAP), pituitary adenylate cyclase‐activating peptide, produced only limited amelioration. As certain genotypes of ApoE increase the probability of Alzheimer's disease, early counseling and preventive treatments may now offer an important route for therapeutics design. © 1997 John Wiley & Sons, Inc. J Neurobiol 33: 329–342, 1997 |
| doi_str_mv | 10.1002/(SICI)1097-4695(199709)33:3<329::AID-NEU10>3.0.CO;2-A |
| format | Article |
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Here, mice deficient in apolipoprotein E (ApoE), a molecule associated with the etiology of Alzheimer's disease, served as a model to investigate the developmental and protective effects of SNV. In comparison to control animals, the deficient mice exhibited (a) reduced amounts of VIP messenger RNA; (b) decreased cholinergic activity (c) significant retardation in the acquisition of developmental milestones: forelimb placing behavior and cliff avoidance behavior; and (d) learning and memory impairments. Daily injections of SNV to ApoE‐deficient newborn pups resulted in increased cholinergic activity and marked improvements in the time of acquisition of behavioral milestones, with peptide‐treated animals developing as fast as control animals and exhibiting improved cognitive functions after cessation of peptide treatment. Specificity was demonstrated in that treatment with a related peptide (PACAP), pituitary adenylate cyclase‐activating peptide, produced only limited amelioration. As certain genotypes of ApoE increase the probability of Alzheimer's disease, early counseling and preventive treatments may now offer an important route for therapeutics design. © 1997 John Wiley & Sons, Inc. J Neurobiol 33: 329–342, 1997</description><identifier>ISSN: 0022-3034</identifier><identifier>EISSN: 1097-4695</identifier><identifier>DOI: 10.1002/(SICI)1097-4695(199709)33:3<329::AID-NEU10>3.0.CO;2-A</identifier><identifier>PMID: 9298769</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Alzheimer Disease - drug therapy ; Animals ; apolipoprotein E ; Apolipoproteins E - deficiency ; Apolipoproteins E - genetics ; Brain - enzymology ; Brain - growth & development ; Brain Diseases - drug therapy ; Brain Diseases - genetics ; Brain Diseases - prevention & control ; Choline O-Acetyltransferase - metabolism ; cholinergic activity ; Cholinergic Fibers - physiology ; developmental milestones ; Learning - drug effects ; learning and memory ; Memory Disorders - drug therapy ; Memory Disorders - genetics ; Memory Disorders - prevention & control ; messenger RNA ; Mice ; Mice, Knockout ; Neuropeptides - pharmacology ; Neuroprotective Agents - pharmacology ; RNA, Messenger - metabolism ; vasoactive intestinal peptide ; Vasoactive Intestinal Peptide - deficiency ; Vasoactive Intestinal Peptide - genetics ; Vasoactive Intestinal Peptide - pharmacology</subject><ispartof>Journal of neurobiology, 1997-09, Vol.33 (3), p.329-342</ispartof><rights>Copyright © 1997 John Wiley & Sons, Inc.</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3630-9518e144ac4189a5c6fabf240f5cf261e3ac476f0ba9954eeb6b11b562d158c23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291097-4695%28199709%2933%3A3%3C329%3A%3AAID-NEU10%3E3.0.CO%3B2-A$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291097-4695%28199709%2933%3A3%3C329%3A%3AAID-NEU10%3E3.0.CO%3B2-A$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27923,27924,45573,45574,46408,46832</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9298769$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gozes, Illana</creatorcontrib><creatorcontrib>Bachar, Michal</creatorcontrib><creatorcontrib>Bardea, Amos</creatorcontrib><creatorcontrib>Davidson, Ariane</creatorcontrib><creatorcontrib>Rubinraut, Sarah</creatorcontrib><creatorcontrib>Fridkin, Mati</creatorcontrib><creatorcontrib>Giladi, Eli</creatorcontrib><title>Protection against developmental retardation in apolipoprotein E‐deficient mice by a fatty neuropeptide: Implications for early treatment of Alzheimer's disease</title><title>Journal of neurobiology</title><addtitle>J Neurobiol</addtitle><description>Stearyl‐Nle‐17‐VIP (SNV) is a novel agonist of vasoactive intestinal peptide (VIP) exhibiting a 100‐fold greater potency than the parent molecule and specificity for a receptor associated with neuronal survival. Here, mice deficient in apolipoprotein E (ApoE), a molecule associated with the etiology of Alzheimer's disease, served as a model to investigate the developmental and protective effects of SNV. In comparison to control animals, the deficient mice exhibited (a) reduced amounts of VIP messenger RNA; (b) decreased cholinergic activity (c) significant retardation in the acquisition of developmental milestones: forelimb placing behavior and cliff avoidance behavior; and (d) learning and memory impairments. Daily injections of SNV to ApoE‐deficient newborn pups resulted in increased cholinergic activity and marked improvements in the time of acquisition of behavioral milestones, with peptide‐treated animals developing as fast as control animals and exhibiting improved cognitive functions after cessation of peptide treatment. Specificity was demonstrated in that treatment with a related peptide (PACAP), pituitary adenylate cyclase‐activating peptide, produced only limited amelioration. As certain genotypes of ApoE increase the probability of Alzheimer's disease, early counseling and preventive treatments may now offer an important route for therapeutics design. © 1997 John Wiley & Sons, Inc. J Neurobiol 33: 329–342, 1997</description><subject>Alzheimer Disease - drug therapy</subject><subject>Animals</subject><subject>apolipoprotein E</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - genetics</subject><subject>Brain - enzymology</subject><subject>Brain - growth & development</subject><subject>Brain Diseases - drug therapy</subject><subject>Brain Diseases - genetics</subject><subject>Brain Diseases - prevention & control</subject><subject>Choline O-Acetyltransferase - metabolism</subject><subject>cholinergic activity</subject><subject>Cholinergic Fibers - physiology</subject><subject>developmental milestones</subject><subject>Learning - drug effects</subject><subject>learning and memory</subject><subject>Memory Disorders - drug therapy</subject><subject>Memory Disorders - genetics</subject><subject>Memory Disorders - prevention & control</subject><subject>messenger RNA</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Neuropeptides - pharmacology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>RNA, Messenger - metabolism</subject><subject>vasoactive intestinal peptide</subject><subject>Vasoactive Intestinal Peptide - deficiency</subject><subject>Vasoactive Intestinal Peptide - genetics</subject><subject>Vasoactive Intestinal Peptide - pharmacology</subject><issn>0022-3034</issn><issn>1097-4695</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctu1DAUhiMEKtPCIyB5Be0igy-5jKeAFIUBIlUMEpSt5TjHYJQbtqcorHgEnoFH40lwZkbdgIS8sHzO7_8_9hdFzwleEozp0_P3VVldEMzzOMl4ek44zzG_YGzNnjHK1-uiehm_3VwT_IIt8bLcXtK4uBMtbm_cjRbBh8YMs-R-dOrcF4wx5yk9iU445as844vo1zs7eFDeDD2Sn6TpnUcN3EA7jB30XrbIgpe2kXuFCaJxaM04jPO1cNz8_vGzAW2UCWrUGQWonpBEWno_oR52dhhh9KaBNaq6sTVq7-SQHiwCadsJeQvSz2Fo0Khov38G04F94lBjHEgHD6J7WrYOHh73s-j61eZD-Sa-2r6uyuIqVixjOOYpWQFJEqkSsuIyVZmWtaYJ1qnSNCPAQifPNK5l-IQEoM5qQuo0ow1JV4qys-jxwTe87esOnBedcQraVvYw7JzIOc2zPJ2FxwGUHZyzoMVoTSftJAgWMzshZnZiJiFmEuLATjAmwqJciMBO7NmFAhblVlBRBN9HxwF2dQfNresRVuh_PPS_mRamv0L_k_mvyEOB_QHGibn9</recordid><startdate>199709</startdate><enddate>199709</enddate><creator>Gozes, Illana</creator><creator>Bachar, Michal</creator><creator>Bardea, Amos</creator><creator>Davidson, Ariane</creator><creator>Rubinraut, Sarah</creator><creator>Fridkin, Mati</creator><creator>Giladi, Eli</creator><general>John Wiley & Sons, Inc</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>7X8</scope></search><sort><creationdate>199709</creationdate><title>Protection against developmental retardation in apolipoprotein E‐deficient mice by a fatty neuropeptide: Implications for early treatment of Alzheimer's disease</title><author>Gozes, Illana ; 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Here, mice deficient in apolipoprotein E (ApoE), a molecule associated with the etiology of Alzheimer's disease, served as a model to investigate the developmental and protective effects of SNV. In comparison to control animals, the deficient mice exhibited (a) reduced amounts of VIP messenger RNA; (b) decreased cholinergic activity (c) significant retardation in the acquisition of developmental milestones: forelimb placing behavior and cliff avoidance behavior; and (d) learning and memory impairments. Daily injections of SNV to ApoE‐deficient newborn pups resulted in increased cholinergic activity and marked improvements in the time of acquisition of behavioral milestones, with peptide‐treated animals developing as fast as control animals and exhibiting improved cognitive functions after cessation of peptide treatment. Specificity was demonstrated in that treatment with a related peptide (PACAP), pituitary adenylate cyclase‐activating peptide, produced only limited amelioration. As certain genotypes of ApoE increase the probability of Alzheimer's disease, early counseling and preventive treatments may now offer an important route for therapeutics design. © 1997 John Wiley & Sons, Inc. J Neurobiol 33: 329–342, 1997</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>9298769</pmid><doi>10.1002/(SICI)1097-4695(199709)33:3<329::AID-NEU10>3.0.CO;2-A</doi><tpages>14</tpages></addata></record> |
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| ispartof | Journal of neurobiology, 1997-09, Vol.33 (3), p.329-342 |
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| subjects | Alzheimer Disease - drug therapy Animals apolipoprotein E Apolipoproteins E - deficiency Apolipoproteins E - genetics Brain - enzymology Brain - growth & development Brain Diseases - drug therapy Brain Diseases - genetics Brain Diseases - prevention & control Choline O-Acetyltransferase - metabolism cholinergic activity Cholinergic Fibers - physiology developmental milestones Learning - drug effects learning and memory Memory Disorders - drug therapy Memory Disorders - genetics Memory Disorders - prevention & control messenger RNA Mice Mice, Knockout Neuropeptides - pharmacology Neuroprotective Agents - pharmacology RNA, Messenger - metabolism vasoactive intestinal peptide Vasoactive Intestinal Peptide - deficiency Vasoactive Intestinal Peptide - genetics Vasoactive Intestinal Peptide - pharmacology |
| title | Protection against developmental retardation in apolipoprotein E‐deficient mice by a fatty neuropeptide: Implications for early treatment of Alzheimer's disease |
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