<\/a><\/p>\n
App<\/em> knock-in mouse strains: new models for\nAlzheimer\u2019s disease<\/b><\/span><\/p>\nC57BL\/6-App<tm1(NL)Tcs><\/i>\/TcsRbrc (RBRC06342)<\/a><\/h5>\nC57BL\/6-App<tm2(NL-F)Tcs><\/i>\/TcsRbrc (RBRC06343)<\/a><\/h5>\nC57BL\/6-App<tm3(NL-G-F)Tcs><\/i>\/TcsRbrc (RBRC06344)<\/a><\/h5>\n<\/a><\/p>\nCourtesy of Takaomi C. Saido, Ph.D. and Takashi Saito, Ph.D.<\/p>\nApp<\/i>\u00a0knock-in mice exhibit AD patient-like A\u03b242<\/sub>-dominant plaque deposition concomitantly with neuroinflammation and memory impairment. Importantly, the mice live normally, in contrast to previous APP overexpression-based models which are aggressive and often die of unknown cause(s).<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nAlzheimer’s disease (AD), which is the major form of dementia, is a syndrome caused by a number of progressive illnesses that affect memory and cognitive capacity. The number of people living with dementia worldwide is estimated at 44 million, and is set to almost double by 2030 if preventive therapies are not found [1]. Researchers have generated a number of transgenic (Tg) mouse models that overexpress human \u03b2 amyloid (A\u03b2) precursor protein (APP); however, these APP-Tg mice showed artificial phenotypes that may have little to do with the human disease.<\/td>\n<\/tr>\n\n\nTakaomi C. Saido, Takashi Saito, and colleagues at RIKEN Brain Science Institute generated App<\/i> knock-in mice with the Swedish mutation (AppNL\/NL<\/sup><\/i>, RBRC06342); Swedish and Iberian mutations (AppNL-F\/NL-F<\/sup><\/i>, RBRC06343); and Swedish, Iberian, and Arctic mutations (AppNL-G-F\/NL-G-F<\/sup><\/i>, RBRC06344) [2-4]. The Swedish KM670\/671NL mutation <\/i>increases the total amount of A\u03b2, while the Beyreuther\/Iberian I716F mutation increases the ratio of A\u03b242<\/sub> to A\u03b240<\/sub>. AppNL-F\/NL-F<\/sup><\/i> mice, which carry the Swedish and Iberian mutations, show A\u03b2 deposition in the cortex and hippocampus at 6 months and memory impairment at 18 months, whereas AppNL\/NL<\/sup><\/i> mice, which carry only the Swedish mutation, are normal. The last group of generated mice, AppNL-G-F\/NL-G-F<\/sup><\/i>, mice carry the Swedish mutation, Iberian mutation, and Arctic E693G mutation, which accelerates A\u03b2 aggregation starting at 2 months and memory impairment at 6 months.<\/p>\n<\/td>\n<\/tr>\n\n\nAppNL-F\/NL-F<\/sup><\/i> and AppNL-G-F\/NL-G-F<\/sup><\/i> mice show typical A\u03b2 pathology, neuroinflammation, and memory impairment, without overexpressing APP or interrupting other mouse genes. These mouse strains will stimulate further research identifying the mechanisms and pathways involved in A\u03b2 amyloidosis. They are listed on the research models database of the web-based scientific community Alzforum [5].<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nDepositor<\/td>\n:<\/td>\nTakaomi C. Saido, Ph.D.<\/b>\n<\/span>Laboratory for Proteolytic Neuroscience,\u00a0RIKEN Brain Science Institute<\/b><\/b><\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm1(NL)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06342<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm2(NL-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06343<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm3(NL-G-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06344<\/td>\n<\/tr>\n\nModel to human diseases<\/td>\n:<\/td>\nALZHEIMER DISEASE; AD\nOMIM ID: 104300\nCEREBRAL AMYLOID ANGIOPATHY, APP-RELATED\nOMIM ID: 605714<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nRIKEN DNA Bank Human Resource \u2013 APP\nRIKEN DNA Bank Mouse Resource \u2013 App<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nDisease-specific (patient-specific) iPS cells\nAlzheimer’s disease, familial type (iPSCs from FAD patients with mutations in presenilin 1 [A246E] and presenilin 2 [N141I])<\/td>\n<\/tr>\n\nReferences<\/td>\n:<\/td>\n[1]<\/td>\nAlzheimer’s\u00a0Disease International\u00a0(ADI).World Alzheimer Report 2014: Dementia and Risk Reduction.<\/a><\/td>\n<\/tr>\n\n[2]<\/td>\nSaito T, Matsuba Y, Mihira N, Takano J, Nilsson P, Itohara S, Iwata N, Saido TC. Single App knock-in mouse models of Alzheimer’s disease.\u00a0Nat Neurosci.<\/em>; 17(5):661-3, 2014.<\/a><\/td>\n<\/tr>\n\n[3]<\/td>\nNew mouse model could revolutionize research in Alzheimer’s disease. RIKEN Press Releases 2014.<\/a><\/td>\n<\/tr>\n\n[4]<\/td>\nNew mouse models raise the bar for Alzheimer’s research. RIKEN Research 2014.<\/a><\/td>\n<\/tr>\n\n[5]<\/td>\nAlzforum website for webinar and information about animal models of Alzheimer\u2019s disease: http:\/\/www.alzforum.org\/.<\/a><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nSeptember 2014\nContact: Shinya Ayabe, Ph.D.<\/a>\nExperimental Animal Division, RIKEN BioResource Center\nAll materials contained on this site may not be reproduced, distributed, displayed, published or broadcast without the prior permission of the owner of that content.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\u00a0<\/span><\/span><\/p>\n <\/p>\n\n\n\n <\/map>\n<\/p>\n <\/p>\n","protected":false},"excerpt":{"rendered":"App knock-in mouse strains: new models for Alzheimer\u2019s disease C57BL\/6-App<tm1(NL)Tcs>\/TcsRbrc (RBRC06342) C57BL\/6-App<tm2(NL-F)Tcs>\/TcsRbrc (RBRC06343) C57BL\/6-App<tm3(NL-G-F)Tcs>\/T […]<\/p>\n","protected":false},"author":19,"featured_media":0,"parent":198,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_seopress_titles_title":"","_seopress_titles_desc":"","_seopress_robots_index":"","_seopress_robots_follow":"","_seopress_robots_imageindex":"","_seopress_robots_snippet":"","_seopress_robots_primary_cat":"","_seopress_robots_breadcrumbs":"","_seopress_robots_freeze_modified_date":"","_seopress_robots_custom_modified_date":"","_seopress_robots_canonical":"","_seopress_social_fb_title":"","_seopress_social_fb_desc":"","_seopress_social_fb_img":"","_seopress_social_fb_img_attachment_id":0,"_seopress_social_fb_img_width":0,"_seopress_social_fb_img_height":0,"_seopress_social_twitter_title":"","_seopress_social_twitter_desc":"","_seopress_social_twitter_img":"","_seopress_social_twitter_img_attachment_id":0,"_seopress_social_twitter_img_width":0,"_seopress_social_twitter_img_height":0,"_seopress_redirections_value":"","_seopress_redirections_enabled":"","_seopress_redirections_enabled_regex":"","_seopress_redirections_logged_status":"","_seopress_redirections_param":"","_seopress_redirections_type":301,"_seopress_analysis_target_kw":"","footnotes":"","_wp_rev_ctl_limit":""},"class_list":["post-11328","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328","targetHints":{"allow":["GET"]}}],"collection":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/users\/19"}],"replies":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/comments?post=11328"}],"version-history":[{"count":20,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions"}],"predecessor-version":[{"id":18579,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions\/18579"}],"up":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/198"}],"wp:attachment":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/media?parent=11328"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
<\/a><\/p>\nCourtesy of Takaomi C. Saido, Ph.D. and Takashi Saito, Ph.D.<\/p>\nApp<\/i>\u00a0knock-in mice exhibit AD patient-like A\u03b242<\/sub>-dominant plaque deposition concomitantly with neuroinflammation and memory impairment. Importantly, the mice live normally, in contrast to previous APP overexpression-based models which are aggressive and often die of unknown cause(s).<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nAlzheimer’s disease (AD), which is the major form of dementia, is a syndrome caused by a number of progressive illnesses that affect memory and cognitive capacity. The number of people living with dementia worldwide is estimated at 44 million, and is set to almost double by 2030 if preventive therapies are not found [1]. Researchers have generated a number of transgenic (Tg) mouse models that overexpress human \u03b2 amyloid (A\u03b2) precursor protein (APP); however, these APP-Tg mice showed artificial phenotypes that may have little to do with the human disease.<\/td>\n<\/tr>\n\n\nTakaomi C. Saido, Takashi Saito, and colleagues at RIKEN Brain Science Institute generated App<\/i> knock-in mice with the Swedish mutation (AppNL\/NL<\/sup><\/i>, RBRC06342); Swedish and Iberian mutations (AppNL-F\/NL-F<\/sup><\/i>, RBRC06343); and Swedish, Iberian, and Arctic mutations (AppNL-G-F\/NL-G-F<\/sup><\/i>, RBRC06344) [2-4]. The Swedish KM670\/671NL mutation <\/i>increases the total amount of A\u03b2, while the Beyreuther\/Iberian I716F mutation increases the ratio of A\u03b242<\/sub> to A\u03b240<\/sub>. AppNL-F\/NL-F<\/sup><\/i> mice, which carry the Swedish and Iberian mutations, show A\u03b2 deposition in the cortex and hippocampus at 6 months and memory impairment at 18 months, whereas AppNL\/NL<\/sup><\/i> mice, which carry only the Swedish mutation, are normal. The last group of generated mice, AppNL-G-F\/NL-G-F<\/sup><\/i>, mice carry the Swedish mutation, Iberian mutation, and Arctic E693G mutation, which accelerates A\u03b2 aggregation starting at 2 months and memory impairment at 6 months.<\/p>\n<\/td>\n<\/tr>\n\n\nAppNL-F\/NL-F<\/sup><\/i> and AppNL-G-F\/NL-G-F<\/sup><\/i> mice show typical A\u03b2 pathology, neuroinflammation, and memory impairment, without overexpressing APP or interrupting other mouse genes. These mouse strains will stimulate further research identifying the mechanisms and pathways involved in A\u03b2 amyloidosis. They are listed on the research models database of the web-based scientific community Alzforum [5].<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nDepositor<\/td>\n:<\/td>\nTakaomi C. Saido, Ph.D.<\/b>\n<\/span>Laboratory for Proteolytic Neuroscience,\u00a0RIKEN Brain Science Institute<\/b><\/b><\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm1(NL)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06342<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm2(NL-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06343<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm3(NL-G-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06344<\/td>\n<\/tr>\n\nModel to human diseases<\/td>\n:<\/td>\nALZHEIMER DISEASE; AD\nOMIM ID: 104300\nCEREBRAL AMYLOID ANGIOPATHY, APP-RELATED\nOMIM ID: 605714<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nRIKEN DNA Bank Human Resource \u2013 APP\nRIKEN DNA Bank Mouse Resource \u2013 App<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nDisease-specific (patient-specific) iPS cells\nAlzheimer’s disease, familial type (iPSCs from FAD patients with mutations in presenilin 1 [A246E] and presenilin 2 [N141I])<\/td>\n<\/tr>\n\nReferences<\/td>\n:<\/td>\n[1]<\/td>\nAlzheimer’s\u00a0Disease International\u00a0(ADI).World Alzheimer Report 2014: Dementia and Risk Reduction.<\/a><\/td>\n<\/tr>\n\n[2]<\/td>\nSaito T, Matsuba Y, Mihira N, Takano J, Nilsson P, Itohara S, Iwata N, Saido TC. Single App knock-in mouse models of Alzheimer’s disease.\u00a0Nat Neurosci.<\/em>; 17(5):661-3, 2014.<\/a><\/td>\n<\/tr>\n\n[3]<\/td>\nNew mouse model could revolutionize research in Alzheimer’s disease. RIKEN Press Releases 2014.<\/a><\/td>\n<\/tr>\n\n[4]<\/td>\nNew mouse models raise the bar for Alzheimer’s research. RIKEN Research 2014.<\/a><\/td>\n<\/tr>\n\n[5]<\/td>\nAlzforum website for webinar and information about animal models of Alzheimer\u2019s disease: http:\/\/www.alzforum.org\/.<\/a><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nSeptember 2014\nContact: Shinya Ayabe, Ph.D.<\/a>\nExperimental Animal Division, RIKEN BioResource Center\nAll materials contained on this site may not be reproduced, distributed, displayed, published or broadcast without the prior permission of the owner of that content.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\u00a0<\/span><\/span><\/p>\n <\/p>\n\n\n\n <\/map>\n<\/p>\n <\/p>\n","protected":false},"excerpt":{"rendered":"App knock-in mouse strains: new models for Alzheimer\u2019s disease C57BL\/6-App<tm1(NL)Tcs>\/TcsRbrc (RBRC06342) C57BL\/6-App<tm2(NL-F)Tcs>\/TcsRbrc (RBRC06343) C57BL\/6-App<tm3(NL-G-F)Tcs>\/T […]<\/p>\n","protected":false},"author":19,"featured_media":0,"parent":198,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_seopress_titles_title":"","_seopress_titles_desc":"","_seopress_robots_index":"","_seopress_robots_follow":"","_seopress_robots_imageindex":"","_seopress_robots_snippet":"","_seopress_robots_primary_cat":"","_seopress_robots_breadcrumbs":"","_seopress_robots_freeze_modified_date":"","_seopress_robots_custom_modified_date":"","_seopress_robots_canonical":"","_seopress_social_fb_title":"","_seopress_social_fb_desc":"","_seopress_social_fb_img":"","_seopress_social_fb_img_attachment_id":0,"_seopress_social_fb_img_width":0,"_seopress_social_fb_img_height":0,"_seopress_social_twitter_title":"","_seopress_social_twitter_desc":"","_seopress_social_twitter_img":"","_seopress_social_twitter_img_attachment_id":0,"_seopress_social_twitter_img_width":0,"_seopress_social_twitter_img_height":0,"_seopress_redirections_value":"","_seopress_redirections_enabled":"","_seopress_redirections_enabled_regex":"","_seopress_redirections_logged_status":"","_seopress_redirections_param":"","_seopress_redirections_type":301,"_seopress_analysis_target_kw":"","footnotes":"","_wp_rev_ctl_limit":""},"class_list":["post-11328","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328","targetHints":{"allow":["GET"]}}],"collection":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/users\/19"}],"replies":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/comments?post=11328"}],"version-history":[{"count":20,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions"}],"predecessor-version":[{"id":18579,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions\/18579"}],"up":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/198"}],"wp:attachment":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/media?parent=11328"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
Courtesy of Takaomi C. Saido, Ph.D. and Takashi Saito, Ph.D.<\/p>\n
App<\/i>\u00a0knock-in mice exhibit AD patient-like A\u03b242<\/sub>-dominant plaque deposition concomitantly with neuroinflammation and memory impairment. Importantly, the mice live normally, in contrast to previous APP overexpression-based models which are aggressive and often die of unknown cause(s).<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nAlzheimer’s disease (AD), which is the major form of dementia, is a syndrome caused by a number of progressive illnesses that affect memory and cognitive capacity. The number of people living with dementia worldwide is estimated at 44 million, and is set to almost double by 2030 if preventive therapies are not found [1]. Researchers have generated a number of transgenic (Tg) mouse models that overexpress human \u03b2 amyloid (A\u03b2) precursor protein (APP); however, these APP-Tg mice showed artificial phenotypes that may have little to do with the human disease.<\/td>\n<\/tr>\n\n\nTakaomi C. Saido, Takashi Saito, and colleagues at RIKEN Brain Science Institute generated App<\/i> knock-in mice with the Swedish mutation (AppNL\/NL<\/sup><\/i>, RBRC06342); Swedish and Iberian mutations (AppNL-F\/NL-F<\/sup><\/i>, RBRC06343); and Swedish, Iberian, and Arctic mutations (AppNL-G-F\/NL-G-F<\/sup><\/i>, RBRC06344) [2-4]. The Swedish KM670\/671NL mutation <\/i>increases the total amount of A\u03b2, while the Beyreuther\/Iberian I716F mutation increases the ratio of A\u03b242<\/sub> to A\u03b240<\/sub>. AppNL-F\/NL-F<\/sup><\/i> mice, which carry the Swedish and Iberian mutations, show A\u03b2 deposition in the cortex and hippocampus at 6 months and memory impairment at 18 months, whereas AppNL\/NL<\/sup><\/i> mice, which carry only the Swedish mutation, are normal. The last group of generated mice, AppNL-G-F\/NL-G-F<\/sup><\/i>, mice carry the Swedish mutation, Iberian mutation, and Arctic E693G mutation, which accelerates A\u03b2 aggregation starting at 2 months and memory impairment at 6 months.<\/p>\n<\/td>\n<\/tr>\n\n\nAppNL-F\/NL-F<\/sup><\/i> and AppNL-G-F\/NL-G-F<\/sup><\/i> mice show typical A\u03b2 pathology, neuroinflammation, and memory impairment, without overexpressing APP or interrupting other mouse genes. These mouse strains will stimulate further research identifying the mechanisms and pathways involved in A\u03b2 amyloidosis. They are listed on the research models database of the web-based scientific community Alzforum [5].<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nDepositor<\/td>\n:<\/td>\nTakaomi C. Saido, Ph.D.<\/b>\n<\/span>Laboratory for Proteolytic Neuroscience,\u00a0RIKEN Brain Science Institute<\/b><\/b><\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm1(NL)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06342<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm2(NL-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06343<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm3(NL-G-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06344<\/td>\n<\/tr>\n\nModel to human diseases<\/td>\n:<\/td>\nALZHEIMER DISEASE; AD\nOMIM ID: 104300\nCEREBRAL AMYLOID ANGIOPATHY, APP-RELATED\nOMIM ID: 605714<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nRIKEN DNA Bank Human Resource \u2013 APP\nRIKEN DNA Bank Mouse Resource \u2013 App<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nDisease-specific (patient-specific) iPS cells\nAlzheimer’s disease, familial type (iPSCs from FAD patients with mutations in presenilin 1 [A246E] and presenilin 2 [N141I])<\/td>\n<\/tr>\n\nReferences<\/td>\n:<\/td>\n[1]<\/td>\nAlzheimer’s\u00a0Disease International\u00a0(ADI).World Alzheimer Report 2014: Dementia and Risk Reduction.<\/a><\/td>\n<\/tr>\n\n[2]<\/td>\nSaito T, Matsuba Y, Mihira N, Takano J, Nilsson P, Itohara S, Iwata N, Saido TC. Single App knock-in mouse models of Alzheimer’s disease.\u00a0Nat Neurosci.<\/em>; 17(5):661-3, 2014.<\/a><\/td>\n<\/tr>\n\n[3]<\/td>\nNew mouse model could revolutionize research in Alzheimer’s disease. RIKEN Press Releases 2014.<\/a><\/td>\n<\/tr>\n\n[4]<\/td>\nNew mouse models raise the bar for Alzheimer’s research. RIKEN Research 2014.<\/a><\/td>\n<\/tr>\n\n[5]<\/td>\nAlzforum website for webinar and information about animal models of Alzheimer\u2019s disease: http:\/\/www.alzforum.org\/.<\/a><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nSeptember 2014\nContact: Shinya Ayabe, Ph.D.<\/a>\nExperimental Animal Division, RIKEN BioResource Center\nAll materials contained on this site may not be reproduced, distributed, displayed, published or broadcast without the prior permission of the owner of that content.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\u00a0<\/span><\/span><\/p>\n <\/p>\n\n\n\n <\/map>\n<\/p>\n <\/p>\n","protected":false},"excerpt":{"rendered":"App knock-in mouse strains: new models for Alzheimer\u2019s disease C57BL\/6-App<tm1(NL)Tcs>\/TcsRbrc (RBRC06342) C57BL\/6-App<tm2(NL-F)Tcs>\/TcsRbrc (RBRC06343) C57BL\/6-App<tm3(NL-G-F)Tcs>\/T […]<\/p>\n","protected":false},"author":19,"featured_media":0,"parent":198,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_seopress_titles_title":"","_seopress_titles_desc":"","_seopress_robots_index":"","_seopress_robots_follow":"","_seopress_robots_imageindex":"","_seopress_robots_snippet":"","_seopress_robots_primary_cat":"","_seopress_robots_breadcrumbs":"","_seopress_robots_freeze_modified_date":"","_seopress_robots_custom_modified_date":"","_seopress_robots_canonical":"","_seopress_social_fb_title":"","_seopress_social_fb_desc":"","_seopress_social_fb_img":"","_seopress_social_fb_img_attachment_id":0,"_seopress_social_fb_img_width":0,"_seopress_social_fb_img_height":0,"_seopress_social_twitter_title":"","_seopress_social_twitter_desc":"","_seopress_social_twitter_img":"","_seopress_social_twitter_img_attachment_id":0,"_seopress_social_twitter_img_width":0,"_seopress_social_twitter_img_height":0,"_seopress_redirections_value":"","_seopress_redirections_enabled":"","_seopress_redirections_enabled_regex":"","_seopress_redirections_logged_status":"","_seopress_redirections_param":"","_seopress_redirections_type":301,"_seopress_analysis_target_kw":"","footnotes":"","_wp_rev_ctl_limit":""},"class_list":["post-11328","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328","targetHints":{"allow":["GET"]}}],"collection":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/users\/19"}],"replies":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/comments?post=11328"}],"version-history":[{"count":20,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions"}],"predecessor-version":[{"id":18579,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions\/18579"}],"up":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/198"}],"wp:attachment":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/media?parent=11328"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
<\/p>\n
Takaomi C. Saido, Takashi Saito, and colleagues at RIKEN Brain Science Institute generated App<\/i> knock-in mice with the Swedish mutation (AppNL\/NL<\/sup><\/i>, RBRC06342); Swedish and Iberian mutations (AppNL-F\/NL-F<\/sup><\/i>, RBRC06343); and Swedish, Iberian, and Arctic mutations (AppNL-G-F\/NL-G-F<\/sup><\/i>, RBRC06344) [2-4]. The Swedish KM670\/671NL mutation <\/i>increases the total amount of A\u03b2, while the Beyreuther\/Iberian I716F mutation increases the ratio of A\u03b242<\/sub> to A\u03b240<\/sub>. AppNL-F\/NL-F<\/sup><\/i> mice, which carry the Swedish and Iberian mutations, show A\u03b2 deposition in the cortex and hippocampus at 6 months and memory impairment at 18 months, whereas AppNL\/NL<\/sup><\/i> mice, which carry only the Swedish mutation, are normal. The last group of generated mice, AppNL-G-F\/NL-G-F<\/sup><\/i>, mice carry the Swedish mutation, Iberian mutation, and Arctic E693G mutation, which accelerates A\u03b2 aggregation starting at 2 months and memory impairment at 6 months.<\/p>\n<\/td>\n<\/tr>\n\n\nAppNL-F\/NL-F<\/sup><\/i> and AppNL-G-F\/NL-G-F<\/sup><\/i> mice show typical A\u03b2 pathology, neuroinflammation, and memory impairment, without overexpressing APP or interrupting other mouse genes. These mouse strains will stimulate further research identifying the mechanisms and pathways involved in A\u03b2 amyloidosis. They are listed on the research models database of the web-based scientific community Alzforum [5].<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nDepositor<\/td>\n:<\/td>\nTakaomi C. Saido, Ph.D.<\/b>\n<\/span>Laboratory for Proteolytic Neuroscience,\u00a0RIKEN Brain Science Institute<\/b><\/b><\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm1(NL)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06342<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm2(NL-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06343<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm3(NL-G-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06344<\/td>\n<\/tr>\n\nModel to human diseases<\/td>\n:<\/td>\nALZHEIMER DISEASE; AD\nOMIM ID: 104300\nCEREBRAL AMYLOID ANGIOPATHY, APP-RELATED\nOMIM ID: 605714<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nRIKEN DNA Bank Human Resource \u2013 APP\nRIKEN DNA Bank Mouse Resource \u2013 App<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nDisease-specific (patient-specific) iPS cells\nAlzheimer’s disease, familial type (iPSCs from FAD patients with mutations in presenilin 1 [A246E] and presenilin 2 [N141I])<\/td>\n<\/tr>\n\nReferences<\/td>\n:<\/td>\n[1]<\/td>\nAlzheimer’s\u00a0Disease International\u00a0(ADI).World Alzheimer Report 2014: Dementia and Risk Reduction.<\/a><\/td>\n<\/tr>\n\n[2]<\/td>\nSaito T, Matsuba Y, Mihira N, Takano J, Nilsson P, Itohara S, Iwata N, Saido TC. Single App knock-in mouse models of Alzheimer’s disease.\u00a0Nat Neurosci.<\/em>; 17(5):661-3, 2014.<\/a><\/td>\n<\/tr>\n\n[3]<\/td>\nNew mouse model could revolutionize research in Alzheimer’s disease. RIKEN Press Releases 2014.<\/a><\/td>\n<\/tr>\n\n[4]<\/td>\nNew mouse models raise the bar for Alzheimer’s research. RIKEN Research 2014.<\/a><\/td>\n<\/tr>\n\n[5]<\/td>\nAlzforum website for webinar and information about animal models of Alzheimer\u2019s disease: http:\/\/www.alzforum.org\/.<\/a><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nSeptember 2014\nContact: Shinya Ayabe, Ph.D.<\/a>\nExperimental Animal Division, RIKEN BioResource Center\nAll materials contained on this site may not be reproduced, distributed, displayed, published or broadcast without the prior permission of the owner of that content.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\u00a0<\/span><\/span><\/p>\n <\/p>\n\n\n\n <\/map>\n<\/p>\n <\/p>\n","protected":false},"excerpt":{"rendered":"App knock-in mouse strains: new models for Alzheimer\u2019s disease C57BL\/6-App<tm1(NL)Tcs>\/TcsRbrc (RBRC06342) C57BL\/6-App<tm2(NL-F)Tcs>\/TcsRbrc (RBRC06343) C57BL\/6-App<tm3(NL-G-F)Tcs>\/T […]<\/p>\n","protected":false},"author":19,"featured_media":0,"parent":198,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_seopress_titles_title":"","_seopress_titles_desc":"","_seopress_robots_index":"","_seopress_robots_follow":"","_seopress_robots_imageindex":"","_seopress_robots_snippet":"","_seopress_robots_primary_cat":"","_seopress_robots_breadcrumbs":"","_seopress_robots_freeze_modified_date":"","_seopress_robots_custom_modified_date":"","_seopress_robots_canonical":"","_seopress_social_fb_title":"","_seopress_social_fb_desc":"","_seopress_social_fb_img":"","_seopress_social_fb_img_attachment_id":0,"_seopress_social_fb_img_width":0,"_seopress_social_fb_img_height":0,"_seopress_social_twitter_title":"","_seopress_social_twitter_desc":"","_seopress_social_twitter_img":"","_seopress_social_twitter_img_attachment_id":0,"_seopress_social_twitter_img_width":0,"_seopress_social_twitter_img_height":0,"_seopress_redirections_value":"","_seopress_redirections_enabled":"","_seopress_redirections_enabled_regex":"","_seopress_redirections_logged_status":"","_seopress_redirections_param":"","_seopress_redirections_type":301,"_seopress_analysis_target_kw":"","footnotes":"","_wp_rev_ctl_limit":""},"class_list":["post-11328","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328","targetHints":{"allow":["GET"]}}],"collection":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/users\/19"}],"replies":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/comments?post=11328"}],"version-history":[{"count":20,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions"}],"predecessor-version":[{"id":18579,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions\/18579"}],"up":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/198"}],"wp:attachment":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/media?parent=11328"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
AppNL-F\/NL-F<\/sup><\/i> and AppNL-G-F\/NL-G-F<\/sup><\/i> mice show typical A\u03b2 pathology, neuroinflammation, and memory impairment, without overexpressing APP or interrupting other mouse genes. These mouse strains will stimulate further research identifying the mechanisms and pathways involved in A\u03b2 amyloidosis. They are listed on the research models database of the web-based scientific community Alzforum [5].<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nDepositor<\/td>\n:<\/td>\nTakaomi C. Saido, Ph.D.<\/b>\n<\/span>Laboratory for Proteolytic Neuroscience,\u00a0RIKEN Brain Science Institute<\/b><\/b><\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm1(NL)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06342<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm2(NL-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06343<\/td>\n<\/tr>\n\nStrain name<\/td>\n:<\/td>\nC57BL\/6-App<tm3(NL-G-F)Tcs><\/i>\/TcsRbrc<\/b><\/span><\/td>\n<\/tr>\n\nRBRC No.<\/td>\n:<\/td>\nRBRC06344<\/td>\n<\/tr>\n\nModel to human diseases<\/td>\n:<\/td>\nALZHEIMER DISEASE; AD\nOMIM ID: 104300\nCEREBRAL AMYLOID ANGIOPATHY, APP-RELATED\nOMIM ID: 605714<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nRIKEN DNA Bank Human Resource \u2013 APP\nRIKEN DNA Bank Mouse Resource \u2013 App<\/td>\n<\/tr>\n\nRelated resources\nfrom RIKEN BRC<\/td>\n:<\/td>\nDisease-specific (patient-specific) iPS cells\nAlzheimer’s disease, familial type (iPSCs from FAD patients with mutations in presenilin 1 [A246E] and presenilin 2 [N141I])<\/td>\n<\/tr>\n\nReferences<\/td>\n:<\/td>\n[1]<\/td>\nAlzheimer’s\u00a0Disease International\u00a0(ADI).World Alzheimer Report 2014: Dementia and Risk Reduction.<\/a><\/td>\n<\/tr>\n\n[2]<\/td>\nSaito T, Matsuba Y, Mihira N, Takano J, Nilsson P, Itohara S, Iwata N, Saido TC. Single App knock-in mouse models of Alzheimer’s disease.\u00a0Nat Neurosci.<\/em>; 17(5):661-3, 2014.<\/a><\/td>\n<\/tr>\n\n[3]<\/td>\nNew mouse model could revolutionize research in Alzheimer’s disease. RIKEN Press Releases 2014.<\/a><\/td>\n<\/tr>\n\n[4]<\/td>\nNew mouse models raise the bar for Alzheimer’s research. RIKEN Research 2014.<\/a><\/td>\n<\/tr>\n\n[5]<\/td>\nAlzforum website for webinar and information about animal models of Alzheimer\u2019s disease: http:\/\/www.alzforum.org\/.<\/a><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n <\/p>\n\n\n\nSeptember 2014\nContact: Shinya Ayabe, Ph.D.<\/a>\nExperimental Animal Division, RIKEN BioResource Center\nAll materials contained on this site may not be reproduced, distributed, displayed, published or broadcast without the prior permission of the owner of that content.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n\u00a0<\/span><\/span><\/p>\n <\/p>\n\n\n\n <\/map>\n<\/p>\n <\/p>\n","protected":false},"excerpt":{"rendered":"App knock-in mouse strains: new models for Alzheimer\u2019s disease C57BL\/6-App<tm1(NL)Tcs>\/TcsRbrc (RBRC06342) C57BL\/6-App<tm2(NL-F)Tcs>\/TcsRbrc (RBRC06343) C57BL\/6-App<tm3(NL-G-F)Tcs>\/T […]<\/p>\n","protected":false},"author":19,"featured_media":0,"parent":198,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_seopress_titles_title":"","_seopress_titles_desc":"","_seopress_robots_index":"","_seopress_robots_follow":"","_seopress_robots_imageindex":"","_seopress_robots_snippet":"","_seopress_robots_primary_cat":"","_seopress_robots_breadcrumbs":"","_seopress_robots_freeze_modified_date":"","_seopress_robots_custom_modified_date":"","_seopress_robots_canonical":"","_seopress_social_fb_title":"","_seopress_social_fb_desc":"","_seopress_social_fb_img":"","_seopress_social_fb_img_attachment_id":0,"_seopress_social_fb_img_width":0,"_seopress_social_fb_img_height":0,"_seopress_social_twitter_title":"","_seopress_social_twitter_desc":"","_seopress_social_twitter_img":"","_seopress_social_twitter_img_attachment_id":0,"_seopress_social_twitter_img_width":0,"_seopress_social_twitter_img_height":0,"_seopress_redirections_value":"","_seopress_redirections_enabled":"","_seopress_redirections_enabled_regex":"","_seopress_redirections_logged_status":"","_seopress_redirections_param":"","_seopress_redirections_type":301,"_seopress_analysis_target_kw":"","footnotes":"","_wp_rev_ctl_limit":""},"class_list":["post-11328","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328","targetHints":{"allow":["GET"]}}],"collection":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/users\/19"}],"replies":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/comments?post=11328"}],"version-history":[{"count":20,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions"}],"predecessor-version":[{"id":18579,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/11328\/revisions\/18579"}],"up":[{"embeddable":true,"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/pages\/198"}],"wp:attachment":[{"href":"http:\/\/mus.brc.riken.jp\/ja\/wp-json\/wp\/v2\/media?parent=11328"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
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