Combination of Insulin with a GLP1 Agonist Is Associated with Better Memory and Normal Expression of Insulin Receptor Pathway Genes in a Mouse Model of Alzheimer’s Disease
Disruption of brain insulin signaling may explain the higher Alzheimer’s disease (AD) risk among type 2 diabetic (T2D) patients. There is evidence from in vitro and human postmortem studies that combination of insulin with hypoglycemic medications is neuroprotective and associated with less amyloid...
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| Veröffentlicht in: | Journal of molecular neuroscience 2019-04, Vol.67 (4), p.504-510 |
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| creator | Robinson, Ari Lubitz, Irit Atrakchi-Baranes, Dana Licht-Murava, Avital Katsel, Pavel Leroith, Derek Liraz-Zaltsman, Sigal Haroutunian, Vahram Beeri, Michal Schnaider |
| description | Disruption of brain insulin signaling may explain the higher Alzheimer’s disease (AD) risk among type 2 diabetic (T2D) patients. There is evidence from in vitro and human postmortem studies that combination of insulin with hypoglycemic medications is neuroprotective and associated with less amyloid aggregation. We examined the effect of 8-month intranasal administration of insulin, exenatide (a GLP-1 agonist), combination therapy (insulin + exenatide) or saline, in wild-type (WT) and an AD-like mouse model (Tg2576). Mice were assessed for learning, gene expression of key mediators and effectors of the insulin receptor signaling pathway (IRSP-IRS1, AKT1, CTNNB1, INSR, IRS2, GSK3B, IGF1R, AKT3), and brain Amyloid Beta (Aβ) levels. In Tg2576 mice, combination therapy reduced expression of IRSP genes which was accompanied by better learning. Cortical Aβ levels were decreased by 15–30% in all groups compared to saline but this difference did not reach statistical significance. WT mice groups, with or without treatment, did not differ in any comparison. Disentangling the mechanisms underlying the potential beneficial effects of combination therapy on the IR pathway and AD-like behavior is warranted. |
| doi_str_mv | 10.1007/s12031-019-1257-9 |
| format | Article |
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There is evidence from in vitro and human postmortem studies that combination of insulin with hypoglycemic medications is neuroprotective and associated with less amyloid aggregation. We examined the effect of 8-month intranasal administration of insulin, exenatide (a GLP-1 agonist), combination therapy (insulin + exenatide) or saline, in wild-type (WT) and an AD-like mouse model (Tg2576). Mice were assessed for learning, gene expression of key mediators and effectors of the insulin receptor signaling pathway (IRSP-IRS1, AKT1, CTNNB1, INSR, IRS2, GSK3B, IGF1R, AKT3), and brain Amyloid Beta (Aβ) levels. In Tg2576 mice, combination therapy reduced expression of IRSP genes which was accompanied by better learning. Cortical Aβ levels were decreased by 15–30% in all groups compared to saline but this difference did not reach statistical significance. WT mice groups, with or without treatment, did not differ in any comparison. Disentangling the mechanisms underlying the potential beneficial effects of combination therapy on the IR pathway and AD-like behavior is warranted.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-019-1257-9</identifier><identifier>PMID: 30635783</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>AKT1 protein ; Alzheimer Disease - drug therapy ; Alzheimer's disease ; Amyloid beta-Peptides - metabolism ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Brain - drug effects ; Brain - metabolism ; Cell Biology ; Cortex ; Diabetes mellitus ; Drug Combinations ; Exenatide - administration & dosage ; Exenatide - pharmacology ; Exenatide - therapeutic use ; Gene expression ; Genes ; GLP-1 receptor agonists ; Health risks ; Hypoglycemic Agents - administration & dosage ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; Insulin ; Insulin - administration & dosage ; Insulin - pharmacology ; Insulin - therapeutic use ; Intranasal administration ; Male ; Maze Learning ; Mice ; Mice, Inbred C57BL ; Neurochemistry ; Neurology ; Neuroprotection ; Neurosciences ; Proteomics ; Receptor, Insulin - metabolism ; Signal Transduction ; Signaling ; Therapy</subject><ispartof>Journal of molecular neuroscience, 2019-04, Vol.67 (4), p.504-510</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Journal of Molecular Neuroscience is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-d1d4a32748f3e41f73dbb465ff5189d6d7616c90aa82975094ceac05fdae36633</citedby><cites>FETCH-LOGICAL-c470t-d1d4a32748f3e41f73dbb465ff5189d6d7616c90aa82975094ceac05fdae36633</cites><orcidid>0000-0002-0330-0207</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-019-1257-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-019-1257-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30635783$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Robinson, Ari</creatorcontrib><creatorcontrib>Lubitz, Irit</creatorcontrib><creatorcontrib>Atrakchi-Baranes, Dana</creatorcontrib><creatorcontrib>Licht-Murava, Avital</creatorcontrib><creatorcontrib>Katsel, Pavel</creatorcontrib><creatorcontrib>Leroith, Derek</creatorcontrib><creatorcontrib>Liraz-Zaltsman, Sigal</creatorcontrib><creatorcontrib>Haroutunian, Vahram</creatorcontrib><creatorcontrib>Beeri, Michal Schnaider</creatorcontrib><title>Combination of Insulin with a GLP1 Agonist Is Associated with Better Memory and Normal Expression of Insulin Receptor Pathway Genes in a Mouse Model of Alzheimer’s Disease</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>Disruption of brain insulin signaling may explain the higher Alzheimer’s disease (AD) risk among type 2 diabetic (T2D) patients. There is evidence from in vitro and human postmortem studies that combination of insulin with hypoglycemic medications is neuroprotective and associated with less amyloid aggregation. We examined the effect of 8-month intranasal administration of insulin, exenatide (a GLP-1 agonist), combination therapy (insulin + exenatide) or saline, in wild-type (WT) and an AD-like mouse model (Tg2576). Mice were assessed for learning, gene expression of key mediators and effectors of the insulin receptor signaling pathway (IRSP-IRS1, AKT1, CTNNB1, INSR, IRS2, GSK3B, IGF1R, AKT3), and brain Amyloid Beta (Aβ) levels. In Tg2576 mice, combination therapy reduced expression of IRSP genes which was accompanied by better learning. Cortical Aβ levels were decreased by 15–30% in all groups compared to saline but this difference did not reach statistical significance. WT mice groups, with or without treatment, did not differ in any comparison. Disentangling the mechanisms underlying the potential beneficial effects of combination therapy on the IR pathway and AD-like behavior is warranted.</description><subject>AKT1 protein</subject><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Cell Biology</subject><subject>Cortex</subject><subject>Diabetes mellitus</subject><subject>Drug Combinations</subject><subject>Exenatide - administration & dosage</subject><subject>Exenatide - pharmacology</subject><subject>Exenatide - therapeutic use</subject><subject>Gene expression</subject><subject>Genes</subject><subject>GLP-1 receptor agonists</subject><subject>Health risks</subject><subject>Hypoglycemic Agents - administration & dosage</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Insulin</subject><subject>Insulin - administration & dosage</subject><subject>Insulin - pharmacology</subject><subject>Insulin - therapeutic use</subject><subject>Intranasal administration</subject><subject>Male</subject><subject>Maze Learning</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>Proteomics</subject><subject>Receptor, Insulin - metabolism</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Therapy</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1ksFu1DAQhiMEotvCA3BBlrhwCdhx4sQXpGUpy0pbqBCcLW8y2XWV2FuPQ7uceA0egpfiSXCUUqASF1vW_83vGc2fJE8YfcEoLV8iyyhnKWUyZVlRpvJeMmNFEV9MiPvJjFaySCshxVFyjHhBacZyVj1MjjgVvCgrPkt-LFy_MVYH4yxxLVlZHDpjyZUJO6LJcn3OyHzrrMFAVkjmiK42OkAzEa8hBPDkDHrnD0Tbhrx3vtcdOb3ee0C84_oRatgH58m5DrsrfSBLsIAkKpqcuQEhng10Y8m8-7oD04P_-e07kjcGQSM8Sh60ukN4fHOfJJ_fnn5avEvXH5arxXyd1nlJQ9qwJtc8K_Oq5ZCztuTNZpOLom0LVslGNKVgopZU6yqTZUFlXoOuadE2GrgQnJ8krybf_bDpoanBBq87tfem1_6gnDbqX8Wandq6L0oUucyliAbPbwy8uxwAg-oN1tB12kKcU2WslFyUeTaiz-6gF27wNo4XKSGyuD42dsQmqvYO0UN72wyjagyDmsKgYhjUGAYlY83Tv6e4rfi9_QhkE4BRslvwf77-v-svcKvCoQ</recordid><startdate>20190401</startdate><enddate>20190401</enddate><creator>Robinson, Ari</creator><creator>Lubitz, Irit</creator><creator>Atrakchi-Baranes, Dana</creator><creator>Licht-Murava, Avital</creator><creator>Katsel, Pavel</creator><creator>Leroith, Derek</creator><creator>Liraz-Zaltsman, Sigal</creator><creator>Haroutunian, Vahram</creator><creator>Beeri, Michal Schnaider</creator><general>Springer US</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>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</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><orcidid>https://orcid.org/0000-0002-0330-0207</orcidid></search><sort><creationdate>20190401</creationdate><title>Combination of Insulin with a GLP1 Agonist Is Associated with Better Memory and Normal Expression of Insulin Receptor Pathway Genes in a Mouse Model of Alzheimer’s Disease</title><author>Robinson, Ari ; Lubitz, Irit ; Atrakchi-Baranes, Dana ; Licht-Murava, Avital ; Katsel, Pavel ; Leroith, Derek ; Liraz-Zaltsman, Sigal ; Haroutunian, Vahram ; Beeri, Michal Schnaider</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-d1d4a32748f3e41f73dbb465ff5189d6d7616c90aa82975094ceac05fdae36633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>AKT1 protein</topic><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Cell Biology</topic><topic>Cortex</topic><topic>Diabetes mellitus</topic><topic>Drug Combinations</topic><topic>Exenatide - administration & dosage</topic><topic>Exenatide - pharmacology</topic><topic>Exenatide - therapeutic use</topic><topic>Gene expression</topic><topic>Genes</topic><topic>GLP-1 receptor agonists</topic><topic>Health risks</topic><topic>Hypoglycemic Agents - administration & dosage</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Insulin</topic><topic>Insulin - administration & dosage</topic><topic>Insulin - pharmacology</topic><topic>Insulin - therapeutic use</topic><topic>Intranasal administration</topic><topic>Male</topic><topic>Maze Learning</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neurosciences</topic><topic>Proteomics</topic><topic>Receptor, Insulin - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Robinson, Ari</au><au>Lubitz, Irit</au><au>Atrakchi-Baranes, Dana</au><au>Licht-Murava, Avital</au><au>Katsel, Pavel</au><au>Leroith, Derek</au><au>Liraz-Zaltsman, Sigal</au><au>Haroutunian, Vahram</au><au>Beeri, Michal Schnaider</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Combination of Insulin with a GLP1 Agonist Is Associated with Better Memory and Normal Expression of Insulin Receptor Pathway Genes in a Mouse Model of Alzheimer’s Disease</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2019-04-01</date><risdate>2019</risdate><volume>67</volume><issue>4</issue><spage>504</spage><epage>510</epage><pages>504-510</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>Disruption of brain insulin signaling may explain the higher Alzheimer’s disease (AD) risk among type 2 diabetic (T2D) patients. There is evidence from in vitro and human postmortem studies that combination of insulin with hypoglycemic medications is neuroprotective and associated with less amyloid aggregation. We examined the effect of 8-month intranasal administration of insulin, exenatide (a GLP-1 agonist), combination therapy (insulin + exenatide) or saline, in wild-type (WT) and an AD-like mouse model (Tg2576). Mice were assessed for learning, gene expression of key mediators and effectors of the insulin receptor signaling pathway (IRSP-IRS1, AKT1, CTNNB1, INSR, IRS2, GSK3B, IGF1R, AKT3), and brain Amyloid Beta (Aβ) levels. In Tg2576 mice, combination therapy reduced expression of IRSP genes which was accompanied by better learning. Cortical Aβ levels were decreased by 15–30% in all groups compared to saline but this difference did not reach statistical significance. WT mice groups, with or without treatment, did not differ in any comparison. Disentangling the mechanisms underlying the potential beneficial effects of combination therapy on the IR pathway and AD-like behavior is warranted.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30635783</pmid><doi>10.1007/s12031-019-1257-9</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-0330-0207</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | AKT1 protein Alzheimer Disease - drug therapy Alzheimer's disease Amyloid beta-Peptides - metabolism Animals Biomedical and Life Sciences Biomedicine Brain Brain - drug effects Brain - metabolism Cell Biology Cortex Diabetes mellitus Drug Combinations Exenatide - administration & dosage Exenatide - pharmacology Exenatide - therapeutic use Gene expression Genes GLP-1 receptor agonists Health risks Hypoglycemic Agents - administration & dosage Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Insulin Insulin - administration & dosage Insulin - pharmacology Insulin - therapeutic use Intranasal administration Male Maze Learning Mice Mice, Inbred C57BL Neurochemistry Neurology Neuroprotection Neurosciences Proteomics Receptor, Insulin - metabolism Signal Transduction Signaling Therapy |
| title | Combination of Insulin with a GLP1 Agonist Is Associated with Better Memory and Normal Expression of Insulin Receptor Pathway Genes in a Mouse Model of Alzheimer’s Disease |
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