Abstract
Commentary on interactions between neurotropic pathogens, neuroinflammatory pathways, and autophagic neural cell death
Highlights
How to cite this article: Cellina M, Orsi M
Even more controversial aspects of autophagy are addressed: first some pathogens, such as herpes simplex viruses, coxsackievirus, listeria monocytogenes have developed strategies to circumvent autophagy-dependent activation of host immune response, some bacteria have the ability to modify the gene transcriptional level of the autophagic process, both in terms of downgrading of autophagy-related genes, as in the case of Yersinia enterocolitica and Francisella tularensis[3], and in terms of up regulation of autophagy-related genes: this mechanism favors a prolonged inflammation at the infection site and results in further injury to surrounding healthy tissues, causing brain matter degeneration
Even if autophagy plays a complex role in Alzheimer’s disease (AD), which needs to be further characterized, the connection between this disease and autophagy dysregulation has been already demonstrated: a pathological accumulation of autophagosomes in neocortical of AD patients has been proved[5] and the mutations of presenilin-1, which are related to AD forms with early-onset, cause a block of the autophagy flux in fibroblasts in these patients[24,25]
Summary
How to cite this article: Cellina M, Orsi M. The activated microglia plays a major role in chronic neuroinflammation, causing long-term cerebral damage by inducing autoimmune reaction, and is observed in various CNS diseases such as stroke, MS, ALS, AD and PD[28].
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