Thalidomide and Lenalidomide Extend Survival in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis
Accumulating evidence suggests that inflammation plays a major role in the pathogenesis of motor neuron death in amyotrophic lateral sclerosis (ALS). Important mediators of inflammation such as the cytokine tumor necrosis factor-alpha (TNF-alpha) and its superfamily member fibroblast-associated cell...
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| Veröffentlicht in: | The Journal of neuroscience 2006-03, Vol.26 (9), p.2467-2473 |
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| creator | Kiaei, Mahmoud Petri, Susanne Kipiani, Khatuna Gardian, Gabrielle Choi, Dong-Kug Chen, Junyu Calingasan, Noel Y Schafer, Peter Muller, George W Stewart, Charles Hensley, Kenneth Beal, M. Flint |
| description | Accumulating evidence suggests that inflammation plays a major role in the pathogenesis of motor neuron death in amyotrophic lateral sclerosis (ALS). Important mediators of inflammation such as the cytokine tumor necrosis factor-alpha (TNF-alpha) and its superfamily member fibroblast-associated cell-surface ligand (FasL) have been implicated in apoptosis. We found increased TNF-alpha and FasL immunoreactivity in lumbar spinal cord sections of ALS patients and G93A transgenic mice. Both increased TNF-alpha and FasL immunostaining in the lumbar spinal cord of the G93A SOD1 transgenic mice occurred at 40-60 d, well before the onset of symptoms and loss of motor neurons. We tested the neuroprotective effect of thalidomide and its analog lenalidomide, pharmacological agents that inhibit the expression of TNF-alpha and other cytokines by destabilizing their mRNA. Treatment with either thalidomide or lenalidomide attenuated weight loss, enhanced motor performance, decreased motor neuron cell death, and significantly increased the life span in G93A transgenic mice. Treated G93A mice showed a reduction in TNF-alpha and FasL immunoreactivity as well as their mRNA in the lumbar spinal cord. Both compounds also reduced interleukin (IL)-12p40, IL-1alpha, and IL-1beta and increased IL-RA and TGF-beta1 mRNA. Therefore, both thalidomide and lenalidomide bear promise as therapeutic interventions for the treatment of ALS. |
| doi_str_mv | 10.1523/JNEUROSCI.5253-05.2006 |
| format | Article |
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Flint</creator><creatorcontrib>Kiaei, Mahmoud ; Petri, Susanne ; Kipiani, Khatuna ; Gardian, Gabrielle ; Choi, Dong-Kug ; Chen, Junyu ; Calingasan, Noel Y ; Schafer, Peter ; Muller, George W ; Stewart, Charles ; Hensley, Kenneth ; Beal, M. Flint</creatorcontrib><description>Accumulating evidence suggests that inflammation plays a major role in the pathogenesis of motor neuron death in amyotrophic lateral sclerosis (ALS). Important mediators of inflammation such as the cytokine tumor necrosis factor-alpha (TNF-alpha) and its superfamily member fibroblast-associated cell-surface ligand (FasL) have been implicated in apoptosis. We found increased TNF-alpha and FasL immunoreactivity in lumbar spinal cord sections of ALS patients and G93A transgenic mice. Both increased TNF-alpha and FasL immunostaining in the lumbar spinal cord of the G93A SOD1 transgenic mice occurred at 40-60 d, well before the onset of symptoms and loss of motor neurons. We tested the neuroprotective effect of thalidomide and its analog lenalidomide, pharmacological agents that inhibit the expression of TNF-alpha and other cytokines by destabilizing their mRNA. Treatment with either thalidomide or lenalidomide attenuated weight loss, enhanced motor performance, decreased motor neuron cell death, and significantly increased the life span in G93A transgenic mice. Treated G93A mice showed a reduction in TNF-alpha and FasL immunoreactivity as well as their mRNA in the lumbar spinal cord. Both compounds also reduced interleukin (IL)-12p40, IL-1alpha, and IL-1beta and increased IL-RA and TGF-beta1 mRNA. Therefore, both thalidomide and lenalidomide bear promise as therapeutic interventions for the treatment of ALS.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/JNEUROSCI.5253-05.2006</identifier><identifier>PMID: 16510725</identifier><language>eng</language><publisher>United States: Soc Neuroscience</publisher><subject>Adult ; Aged ; Amyotrophic Lateral Sclerosis - drug therapy ; Amyotrophic Lateral Sclerosis - metabolism ; Amyotrophic Lateral Sclerosis - mortality ; Analysis of Variance ; Animals ; Cell Count ; Cytokines - metabolism ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Fas Ligand Protein ; Female ; Fluorescent Antibody Technique - methods ; Glial Fibrillary Acidic Protein - metabolism ; Humans ; Immunosuppressive Agents - therapeutic use ; Male ; Membrane Glycoproteins - metabolism ; Mice ; Mice, Transgenic ; Middle Aged ; Motor Activity - drug effects ; Motor Activity - physiology ; Neurons - pathology ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - metabolism ; Rotarod Performance Test - methods ; Superoxide Dismutase - genetics ; Survival ; Thalidomide - analogs & derivatives ; Thalidomide - therapeutic use ; Time Factors ; Tumor Necrosis Factor-alpha - metabolism ; Tumor Necrosis Factors - metabolism</subject><ispartof>The Journal of neuroscience, 2006-03, Vol.26 (9), p.2467-2473</ispartof><rights>Copyright © 2006 Society for Neuroscience 0270-6474/06/262467-07$15.00/0 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c593t-f7c1f511302ba8ce07190c7c0f811a509eb82c612a00c98e30b0db914e4cb0713</citedby><cites>FETCH-LOGICAL-c593t-f7c1f511302ba8ce07190c7c0f811a509eb82c612a00c98e30b0db914e4cb0713</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/PMC6793668/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6793668/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16510725$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kiaei, Mahmoud</creatorcontrib><creatorcontrib>Petri, Susanne</creatorcontrib><creatorcontrib>Kipiani, Khatuna</creatorcontrib><creatorcontrib>Gardian, Gabrielle</creatorcontrib><creatorcontrib>Choi, Dong-Kug</creatorcontrib><creatorcontrib>Chen, Junyu</creatorcontrib><creatorcontrib>Calingasan, Noel Y</creatorcontrib><creatorcontrib>Schafer, Peter</creatorcontrib><creatorcontrib>Muller, George W</creatorcontrib><creatorcontrib>Stewart, Charles</creatorcontrib><creatorcontrib>Hensley, Kenneth</creatorcontrib><creatorcontrib>Beal, M. Flint</creatorcontrib><title>Thalidomide and Lenalidomide Extend Survival in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>Accumulating evidence suggests that inflammation plays a major role in the pathogenesis of motor neuron death in amyotrophic lateral sclerosis (ALS). Important mediators of inflammation such as the cytokine tumor necrosis factor-alpha (TNF-alpha) and its superfamily member fibroblast-associated cell-surface ligand (FasL) have been implicated in apoptosis. We found increased TNF-alpha and FasL immunoreactivity in lumbar spinal cord sections of ALS patients and G93A transgenic mice. Both increased TNF-alpha and FasL immunostaining in the lumbar spinal cord of the G93A SOD1 transgenic mice occurred at 40-60 d, well before the onset of symptoms and loss of motor neurons. We tested the neuroprotective effect of thalidomide and its analog lenalidomide, pharmacological agents that inhibit the expression of TNF-alpha and other cytokines by destabilizing their mRNA. Treatment with either thalidomide or lenalidomide attenuated weight loss, enhanced motor performance, decreased motor neuron cell death, and significantly increased the life span in G93A transgenic mice. Treated G93A mice showed a reduction in TNF-alpha and FasL immunoreactivity as well as their mRNA in the lumbar spinal cord. Both compounds also reduced interleukin (IL)-12p40, IL-1alpha, and IL-1beta and increased IL-RA and TGF-beta1 mRNA. Therefore, both thalidomide and lenalidomide bear promise as therapeutic interventions for the treatment of ALS.</description><subject>Adult</subject><subject>Aged</subject><subject>Amyotrophic Lateral Sclerosis - drug therapy</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Amyotrophic Lateral Sclerosis - mortality</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Cell Count</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fas Ligand Protein</subject><subject>Female</subject><subject>Fluorescent Antibody Technique - methods</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Humans</subject><subject>Immunosuppressive Agents - therapeutic use</subject><subject>Male</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Middle Aged</subject><subject>Motor Activity - drug effects</subject><subject>Motor Activity - physiology</subject><subject>Neurons - pathology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - metabolism</subject><subject>Rotarod Performance Test - methods</subject><subject>Superoxide Dismutase - genetics</subject><subject>Survival</subject><subject>Thalidomide - analogs & derivatives</subject><subject>Thalidomide - therapeutic use</subject><subject>Time Factors</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor Necrosis Factors - metabolism</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUU2P0zAQtRCILQt_YZUTt5SxHdvxBWlVFVhUWIl2z5bjTBqjfBQ7bdl_j6uttnDiYkvzPvRmHiE3FOZUMP7h6_flw4_79eJuLpjgOYg5A5AvyCyhOmcF0JdkBkxBLgtVXJE3Mf4EAAVUvSZXVAoKiokZ8ZvWdr4ee19jZoc6W-FwGSx_T5hm6304-IPtMj9kNtsEO8QtDt5l38Z9xPTW2GVjk932j-MUxl2boJWdMCTJ2nUYxujjW_KqsV3Ed-f_mjx8Wm4WX_LV_ee7xe0qd0LzKW-Uo42glAOrbOkQFNXglIOmpNQK0FiVzEnKLIDTJXKooK40LbBwVSLza_LxyXe3r3qsHQ5TymF2wfc2PJrRevMvMvjWbMeDkUpzKctk8P5sEMZfe4yT6X102HV2wLRv4ilKNSv-S6S65BykTET5RHTpEjFg85yGgjnVaZ7rNKc6DQhzqjMJb_7e5SI793eJ0Ppte_QBText1yU6NcfjkUmjDSuk4n8AwqGrlA</recordid><startdate>20060301</startdate><enddate>20060301</enddate><creator>Kiaei, Mahmoud</creator><creator>Petri, Susanne</creator><creator>Kipiani, Khatuna</creator><creator>Gardian, Gabrielle</creator><creator>Choi, Dong-Kug</creator><creator>Chen, Junyu</creator><creator>Calingasan, Noel Y</creator><creator>Schafer, Peter</creator><creator>Muller, George W</creator><creator>Stewart, Charles</creator><creator>Hensley, Kenneth</creator><creator>Beal, M. 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Flint</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thalidomide and Lenalidomide Extend Survival in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2006-03-01</date><risdate>2006</risdate><volume>26</volume><issue>9</issue><spage>2467</spage><epage>2473</epage><pages>2467-2473</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>Accumulating evidence suggests that inflammation plays a major role in the pathogenesis of motor neuron death in amyotrophic lateral sclerosis (ALS). Important mediators of inflammation such as the cytokine tumor necrosis factor-alpha (TNF-alpha) and its superfamily member fibroblast-associated cell-surface ligand (FasL) have been implicated in apoptosis. We found increased TNF-alpha and FasL immunoreactivity in lumbar spinal cord sections of ALS patients and G93A transgenic mice. Both increased TNF-alpha and FasL immunostaining in the lumbar spinal cord of the G93A SOD1 transgenic mice occurred at 40-60 d, well before the onset of symptoms and loss of motor neurons. We tested the neuroprotective effect of thalidomide and its analog lenalidomide, pharmacological agents that inhibit the expression of TNF-alpha and other cytokines by destabilizing their mRNA. Treatment with either thalidomide or lenalidomide attenuated weight loss, enhanced motor performance, decreased motor neuron cell death, and significantly increased the life span in G93A transgenic mice. Treated G93A mice showed a reduction in TNF-alpha and FasL immunoreactivity as well as their mRNA in the lumbar spinal cord. Both compounds also reduced interleukin (IL)-12p40, IL-1alpha, and IL-1beta and increased IL-RA and TGF-beta1 mRNA. Therefore, both thalidomide and lenalidomide bear promise as therapeutic interventions for the treatment of ALS.</abstract><cop>United States</cop><pub>Soc Neuroscience</pub><pmid>16510725</pmid><doi>10.1523/JNEUROSCI.5253-05.2006</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Amyotrophic Lateral Sclerosis - drug therapy Amyotrophic Lateral Sclerosis - metabolism Amyotrophic Lateral Sclerosis - mortality Analysis of Variance Animals Cell Count Cytokines - metabolism Disease Models, Animal Dose-Response Relationship, Drug Fas Ligand Protein Female Fluorescent Antibody Technique - methods Glial Fibrillary Acidic Protein - metabolism Humans Immunosuppressive Agents - therapeutic use Male Membrane Glycoproteins - metabolism Mice Mice, Transgenic Middle Aged Motor Activity - drug effects Motor Activity - physiology Neurons - pathology Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - metabolism Rotarod Performance Test - methods Superoxide Dismutase - genetics Survival Thalidomide - analogs & derivatives Thalidomide - therapeutic use Time Factors Tumor Necrosis Factor-alpha - metabolism Tumor Necrosis Factors - metabolism |
| title | Thalidomide and Lenalidomide Extend Survival in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis |
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