Welton Daniel Nogueira Godinho, Francisco Sérgio Lopes Vasconcelos Filho, Daniel Vieira Pinto, Juliana Osório Alves, Tyciane de Souza Nascimento, Isabele Dutra de Aguiar, Guilherme Nizan Silva Almeida, Vânia Marilande Ceccatto, Paula Matias Soares
{"title":"高强度间歇训练可预防阿尔茨海默病大鼠模型的认知功能受损并增加肌肉基因 Fndc5 和 Ppargc1a 的表达。","authors":"Welton Daniel Nogueira Godinho, Francisco Sérgio Lopes Vasconcelos Filho, Daniel Vieira Pinto, Juliana Osório Alves, Tyciane de Souza Nascimento, Isabele Dutra de Aguiar, Guilherme Nizan Silva Almeida, Vânia Marilande Ceccatto, Paula Matias Soares","doi":"10.2174/1567205020666221207103109","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease is the most common neurodegenerative disease in the world, characterized by the progressive loss of neuronal structure and function, whose main histopathological landmark is the accumulation of β-amyloid in the brain.</p><p><strong>Objective: </strong>It is well known that exercise is a neuroprotective factor and that muscles produce and release myokines that exert endocrine effects in inflammation and metabolic dysfunction. Thus, this work intends to establish the relationship between the benefits of exercise through the chronic training of HIIT on cognitive damage induced by the Alzheimer's model by the injection of β amyloid<sub>1-42</sub>.</p><p><strong>Methods: </strong>For this purpose, forty-eight male Wistar rats were divided into four groups: Sedentary Sham (SS), Trained Sham (ST), Sedentary Alzheimer's (AS), and Trained Alzheimer's (AT). Animals were submitted to stereotactic surgery and received a hippocampal injection of Aβ<sub>1-42</sub> or a saline solution. Seven days after surgery, twelve days of treadmill adaptation followed by five maximal running tests (MRT) and fifty-five days of HIIT, rats underwent the Morris water maze test. The animals were then euthanized, and their gastrocnemius muscle tissue was extracted to analyze the Fibronectin type III domain containing 5 (FNDC5), PPARG Coactivator 1 Alpha (PPARGC1A), and Integrin subunit beta 5 (ITGB5-R) expression by qRT-PCR in addition to cross-sectional areas.</p><p><strong>Results: </strong>The HIIT prevents the cognitive deficit induced by the infusion of amyloid β<sub>1-42</sub> (p < 0.0001), causes adaptation of muscle fibers (p < 0.0001), modulates the gene expression of FNDC5 (p < 0.01), ITGB5 (p < 0.01) and PPARGC1A (p < 0.01), and induces an increase in peripheral protein expression of FNDC5 (p < 0.005).</p><p><strong>Conclusion: </strong>Thus, we conclude that HIIT can prevent cognitive damage induced by the infusion of Aβ<sub>1-42</sub>, constituting a non-pharmacological tool that modulates important genetic and protein pathways.</p>","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":" ","pages":"830-840"},"PeriodicalIF":1.8000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"High-Intense Interval Training Prevents Cognitive Impairment and Increases the Expression of Muscle Genes FNDC5 and PPARGC1A in a Rat Model of Alzheimer's Disease.\",\"authors\":\"Welton Daniel Nogueira Godinho, Francisco Sérgio Lopes Vasconcelos Filho, Daniel Vieira Pinto, Juliana Osório Alves, Tyciane de Souza Nascimento, Isabele Dutra de Aguiar, Guilherme Nizan Silva Almeida, Vânia Marilande Ceccatto, Paula Matias Soares\",\"doi\":\"10.2174/1567205020666221207103109\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Alzheimer's disease is the most common neurodegenerative disease in the world, characterized by the progressive loss of neuronal structure and function, whose main histopathological landmark is the accumulation of β-amyloid in the brain.</p><p><strong>Objective: </strong>It is well known that exercise is a neuroprotective factor and that muscles produce and release myokines that exert endocrine effects in inflammation and metabolic dysfunction. Thus, this work intends to establish the relationship between the benefits of exercise through the chronic training of HIIT on cognitive damage induced by the Alzheimer's model by the injection of β amyloid<sub>1-42</sub>.</p><p><strong>Methods: </strong>For this purpose, forty-eight male Wistar rats were divided into four groups: Sedentary Sham (SS), Trained Sham (ST), Sedentary Alzheimer's (AS), and Trained Alzheimer's (AT). Animals were submitted to stereotactic surgery and received a hippocampal injection of Aβ<sub>1-42</sub> or a saline solution. Seven days after surgery, twelve days of treadmill adaptation followed by five maximal running tests (MRT) and fifty-five days of HIIT, rats underwent the Morris water maze test. The animals were then euthanized, and their gastrocnemius muscle tissue was extracted to analyze the Fibronectin type III domain containing 5 (FNDC5), PPARG Coactivator 1 Alpha (PPARGC1A), and Integrin subunit beta 5 (ITGB5-R) expression by qRT-PCR in addition to cross-sectional areas.</p><p><strong>Results: </strong>The HIIT prevents the cognitive deficit induced by the infusion of amyloid β<sub>1-42</sub> (p < 0.0001), causes adaptation of muscle fibers (p < 0.0001), modulates the gene expression of FNDC5 (p < 0.01), ITGB5 (p < 0.01) and PPARGC1A (p < 0.01), and induces an increase in peripheral protein expression of FNDC5 (p < 0.005).</p><p><strong>Conclusion: </strong>Thus, we conclude that HIIT can prevent cognitive damage induced by the infusion of Aβ<sub>1-42</sub>, constituting a non-pharmacological tool that modulates important genetic and protein pathways.</p>\",\"PeriodicalId\":10810,\"journal\":{\"name\":\"Current Alzheimer research\",\"volume\":\" \",\"pages\":\"830-840\"},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2022-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current Alzheimer research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2174/1567205020666221207103109\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Alzheimer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/1567205020666221207103109","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
High-Intense Interval Training Prevents Cognitive Impairment and Increases the Expression of Muscle Genes FNDC5 and PPARGC1A in a Rat Model of Alzheimer's Disease.
Background: Alzheimer's disease is the most common neurodegenerative disease in the world, characterized by the progressive loss of neuronal structure and function, whose main histopathological landmark is the accumulation of β-amyloid in the brain.
Objective: It is well known that exercise is a neuroprotective factor and that muscles produce and release myokines that exert endocrine effects in inflammation and metabolic dysfunction. Thus, this work intends to establish the relationship between the benefits of exercise through the chronic training of HIIT on cognitive damage induced by the Alzheimer's model by the injection of β amyloid1-42.
Methods: For this purpose, forty-eight male Wistar rats were divided into four groups: Sedentary Sham (SS), Trained Sham (ST), Sedentary Alzheimer's (AS), and Trained Alzheimer's (AT). Animals were submitted to stereotactic surgery and received a hippocampal injection of Aβ1-42 or a saline solution. Seven days after surgery, twelve days of treadmill adaptation followed by five maximal running tests (MRT) and fifty-five days of HIIT, rats underwent the Morris water maze test. The animals were then euthanized, and their gastrocnemius muscle tissue was extracted to analyze the Fibronectin type III domain containing 5 (FNDC5), PPARG Coactivator 1 Alpha (PPARGC1A), and Integrin subunit beta 5 (ITGB5-R) expression by qRT-PCR in addition to cross-sectional areas.
Results: The HIIT prevents the cognitive deficit induced by the infusion of amyloid β1-42 (p < 0.0001), causes adaptation of muscle fibers (p < 0.0001), modulates the gene expression of FNDC5 (p < 0.01), ITGB5 (p < 0.01) and PPARGC1A (p < 0.01), and induces an increase in peripheral protein expression of FNDC5 (p < 0.005).
Conclusion: Thus, we conclude that HIIT can prevent cognitive damage induced by the infusion of Aβ1-42, constituting a non-pharmacological tool that modulates important genetic and protein pathways.
期刊介绍：
Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer''s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ''bird''s-eye view'' of the current state of Alzheimer''s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.
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