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Age-dependent neurodegenerative disorders are a set of diseases that affect millions of individuals worldwide. Apart from a small subset that are the result of well-defined inherited autosomal dominant gene mutations (e.g., those encoding the β-amyloid precursor protein and presenilins), our understanding of the genetic network that underscores their pathology, remains scarce. Genome-wide association studies (GWAS) especially in Alzheimer's disease patients and research in Parkinson's disease have implicated inflammation and the innate immune response as risk factors. However, even if GWAS etiology points toward innate immunity, untangling cause, and consequence is a challenging task. Specifically, it is not clear whether predisposition to de-regulated immunity causes an inadequate response to protein aggregation (such as amyloid or α-synuclein) or is the direct cause of this aggregation. Given the evolutionary conservation of the innate immune response in Drosophila and humans, unraveling whether hyperactive immune response in glia have a protective or pathological role in the brain could be a potential strategy in combating age-related neurological diseases.

Original publication

DOI

10.3389/fimmu.2020.01574

Type

Journal article

Journal

Front Immunol

Publication Date

2020

Volume

11

Keywords

aging, drosophila, immunity, immunotherapy, neurodegeneration, Age Factors, Aging, Animals, Autophagy, Biomarkers, Disease Models, Animal, Disease Susceptibility, Drosophila, Humans, Immunity, Immunomodulation, Neurodegenerative Diseases, Neuroprotection