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JOURNAL ARTICLE
REVIEW
Inflammation, a significant player of Ataxia-Telangiectasia pathogenesis?
Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.] 2018 July
INTRODUCTION: Ataxia-Telangiectasia (A-T) syndrome is an autosomal recessive neurodegenerative disorder characterized by cerebellar ataxia, oculocutaneous telangiectasia, immunodeficiency, chromosome instability, radiosensitivity, and predisposition to malignancy. There is growing evidence that A-T patients suffer from pathologic inflammation that is responsible for many symptoms of this syndrome, including neurodegeneration, autoimmunity, cardiovascular disease, accelerated aging, and insulin resistance. In addition, epidemiological studies have shown A-T heterozygotes, somewhat like deficient patients, are susceptible to ionizing irradiation and have a higher risk of cancers and metabolic disorders.
AREA COVERED: This review summarizes clinical and molecular findings of inflammation in A-T syndrome.
CONCLUSION: Ataxia-Telangiectasia Mutated (ATM), a master regulator of the DNA damage response is the protein known to be associated with A-T and has a complex nuclear and cytoplasmic role. Loss of ATM function may induce immune deregulation and systemic inflammation.
AREA COVERED: This review summarizes clinical and molecular findings of inflammation in A-T syndrome.
CONCLUSION: Ataxia-Telangiectasia Mutated (ATM), a master regulator of the DNA damage response is the protein known to be associated with A-T and has a complex nuclear and cytoplasmic role. Loss of ATM function may induce immune deregulation and systemic inflammation.
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