Identifying New Immunomodulatory Targets for Alzheimers and Other Neurodegenerative Diseases

确定阿尔茨海默病和其他神经退行性疾病的新免疫调节靶点

• 批准号: 9766179
• 负责人: Benjamin Jacob Doranz
• 金额: $ 20.38万
• 依托单位: INTEGRAL MOLECULAR
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-09-01 至 2022-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9766179
• 关键词: Abbreviations; Alzheimer' s Disease; American; Antibodies; Area; Astrocytes; Binding; Biosensor; Cause of Death; Cells; Clinical Trials; Communication; Disease; Disease Progression; Generations; Genetic; Goals; Health; Human; Immune; Immunooncology; Intervention; Ligands; Link; Membrane; Membrane Proteins; Microglia; Molecular; Molecular Conformation; Neurodegenerative Disorders; Neurofibrillary Tangles; Neuroimmune; Pathologic; Pharmaceutical Preparations; Phenotype; Prevalence; Process; Proteins; Proteome; Receptor Cell; Risk; Senile Plaques; Specificity; Structure; Surface; T-Lymphocyte; Technology; Testing; Therapeutic; Therapeutic Clinical Trial; TimeLine; Titrations; Treatment Efficacy; Virus Receptors; Work; cell type; disability; effective therapy; experimental study; genome wide association study; immune checkpoint; immunoregulation; neuroregulation; new therapeutic target; novel; oncology; prevent; receptor; response; risk minimization; screening; tau Proteins; therapeutic target; therapy development

ABSTRACT Alzheimer's disease (AD) and other neurodegenerative diseases are a major cause of death and disability for older Americans, with a US prevalence of more than 6.5 million. As AD currently cannot be cured or prevented, there is an urgent need for effective treatments targeting underlying disease processes. A major roadblock in treatment development has been the lack of good targets. Although pathologically important, amyloid beta plaques and tau tangles are not easily druggable, and clinical trials of therapeutics targeting these proteins directly have largely failed. Recent genome-wide association studies have identified a link between a growing number of modulatory proteins on neuroimmune cells, particularly on the surface of microglia and astrocytes, that are linked to the risk of developing AD. The identification of new proteins with neuroimmunomodulatory activities could enable an entirely new generation of therapeutic targets with the potential to treat, delay, and possibly even prevent AD and other neurodegenerative diseases.

摘要