The 21st century epidemic: infections as inductors of neuro-degeneration associated with Alzheimer’s Disease

Immunity & Ageing

Elisa Porcellini¹  Elena Raschi¹  Ilaria Carbone¹  Federico Licastro² 

[1] Department of Experimental, Diagnostic and Specialty Medicine, School of Medicine, University of Bologna, Bologna 40100, Italy;Laboratory of Immunopathology and Immunogenetics, Department of Experimental, Diagnostic and Specialty Medicine, School of Medicine, University of Bologna, Via S. Giacomo 14, Bologna, 40126, Italy

关键词: Inflammatory markers and cognitive decline;    Neuro-inflammation;    Peripheral inflammation;    Herpes virus latency;    Alzheimer’s disease;   

Others  :  1133787
DOI  :  10.1186/s12979-014-0022-8

 received in 2014-10-31, accepted in 2014-11-22,  发布年份 2014

【 摘 要 】

Alzheimer’s disease (AD) is a complex disease resulting in neurodegeneration and cognitive impairment. Investigations on environmental factors implicated in AD are scarce and the etiology of the disease remains up to now obscure. The disease’s pathogenesis may be multi-factorial and different etiological factors may converge during aging and induce an activation of brain microglia and macrophages. This microglia priming will result in chronic neuro-inflammation under chronic antigen activation. Infective agents may prime and drive iper-activation of microglia and be partially responsible of the induction of brain inflammation and decline of cognitive performances. Age-associated immune dis-functions induced by chronic sub-clinical infections appear to substantially contribute to the appearance of neuro-inflammation in the elderly. Individual predisposition to less efficient immune responses is another relevant factor contributing to impaired regulation of inflammatory responses and accelerated cognitive decline.

Life-long virus infection may play a pivotal role in activating peripheral and central inflammatory responses and in turn contributing to increased cognitive impairment in preclinical and clinical AD.

【 授权许可】

   
2014 Licastro et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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