Research Topic

The Neuroimmune System in Alzheimer’s Disease

About this Research Topic

The brain's immune system has long been implicated as a key factor in the pathogenesis of Alzheimer’s disease (AD), in particular, activation of microglia was shown to play a role in the development and progression of the disease. Nonetheless, AD research has been, in large part, dedicated to the exploration of the pathological hallmarks, amyloid beta (Aβ) plaques, neurofibrillary tangles (NFT).

Over the past decade, numerous variants in immune response-related genes have been identified in whole-genome sequencing and GWAS analyses of late onset AD (LOAD). These genes are involved in a wide range of immune-related functions indicating that neuroinflammation plays a critical role in LOAD development. The LOAD genetic discoveries shift the paradigm of AD research towards the understanding of the underpinning immune mechanisms of the disease. Emerging data from functional genomic studies, novel bioinformatics tools, and innovative model systems provide an increasing amount of evidence for genetic, molecular, and cellular changes in the immune response that are associated with LOAD. Thus, providing strong support for an innate immune contribution to disease pathology. Understanding what the role of the immune system in LOAD is, will allow researchers to better understand how to target this system more accurately in order to try and prevent a key early-stage disease process. These advances may lead to the development of new therapeutic targets and disease biomarkers based on immune response pathways.

The topics we would like to cover in this article collection include but are not limited to:

• The identification of immune-related genes through LOAD GWAS, whole genome and exon sequencing analyses
• LOAD associated differential gene expression in cells of the myeloid lineage including microglia
• Mechanistic insight into the function of LOAD-associated immune response genes such as TREM2 and SPI1
• Functional and integrative genomics pointing at the involvement of innate immunity and neuroinflammation in AD
• Animal models developed to investigate the role of the innate immune system in AD
• hiPSC-derived microglial models for the study of AD
• Dysregulation of the central nervous system (CNS) immune response and the role of microglia in AD
• The peripheral immune system in aging and AD
• Application for the development of biomarkers for early diagnosis of AD
• Immune modifying therapies for AD


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

The brain's immune system has long been implicated as a key factor in the pathogenesis of Alzheimer’s disease (AD), in particular, activation of microglia was shown to play a role in the development and progression of the disease. Nonetheless, AD research has been, in large part, dedicated to the exploration of the pathological hallmarks, amyloid beta (Aβ) plaques, neurofibrillary tangles (NFT).

Over the past decade, numerous variants in immune response-related genes have been identified in whole-genome sequencing and GWAS analyses of late onset AD (LOAD). These genes are involved in a wide range of immune-related functions indicating that neuroinflammation plays a critical role in LOAD development. The LOAD genetic discoveries shift the paradigm of AD research towards the understanding of the underpinning immune mechanisms of the disease. Emerging data from functional genomic studies, novel bioinformatics tools, and innovative model systems provide an increasing amount of evidence for genetic, molecular, and cellular changes in the immune response that are associated with LOAD. Thus, providing strong support for an innate immune contribution to disease pathology. Understanding what the role of the immune system in LOAD is, will allow researchers to better understand how to target this system more accurately in order to try and prevent a key early-stage disease process. These advances may lead to the development of new therapeutic targets and disease biomarkers based on immune response pathways.

The topics we would like to cover in this article collection include but are not limited to:

• The identification of immune-related genes through LOAD GWAS, whole genome and exon sequencing analyses
• LOAD associated differential gene expression in cells of the myeloid lineage including microglia
• Mechanistic insight into the function of LOAD-associated immune response genes such as TREM2 and SPI1
• Functional and integrative genomics pointing at the involvement of innate immunity and neuroinflammation in AD
• Animal models developed to investigate the role of the innate immune system in AD
• hiPSC-derived microglial models for the study of AD
• Dysregulation of the central nervous system (CNS) immune response and the role of microglia in AD
• The peripheral immune system in aging and AD
• Application for the development of biomarkers for early diagnosis of AD
• Immune modifying therapies for AD


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

30 June 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

30 June 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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