Oral microbiota and Alzheimer's disease: Do all roads lead to Rome?

Alzheimer's disease (AD) is a progressive neurodegenerative pathology affecting milions of people worldwide associated with deposition of senile plaques. While the genetic and environmental risk factors associated with the onset and consolidation of late onset AD are heterogeneous and sporadic, growing evidence also suggests a potential link between some infectious diseases caused by oral microbiota and AD. Oral microbiota dysbiosis is purported to contribute either directly to amyloid protein production, or indirectly to neuroinflammation, occurring as a consequence of bacterial invasion. Over the last decade, the development of Human Oral Microbiome database (HOMD) has deepened our understanding of oral microbes and their different roles during the human lifetime. Oral pathogens mostly cause caries, periodontal disease, and edentulism in aged population, and, in particular, alterations of the oral microbiota causing chronic periodontal disease have been associated with the risk of AD. Here we describe how different alterations of the oral microbiota may be linked to AD, highlighting the importance of a good oral hygiene for the prevention of oral microbiota dysbiosis.

Targeting STATs in neuroinflammation: The road less traveled!

JAK/STAT transduction pathway is a highly conserved pathway implicated in regulating cellular proliferation, differentiation, survival and apoptosis. Dysregulation of this pathway is involved in the onset of autoimmune, haematological, oncological, metabolic and neurological diseases. Over the last few years, the research of anti-neuroinflammatory agents has gained considerable attention. The ability to diminish the STAT-induced transcription of inflammatory genes is documented for both natural compounds (such as polyphenols) and chemical drugs. Among polyphenols, quercetin and curcumin directly inhibit STAT, while Berberis vulgaris L. and Sophora alopecuroides L extracts act indirectly. Also, the Food and Drug Administration has approved several JAK/STAT inhibitors (direct or indirect) for treating inflammatory diseases, indicating STAT can be considered as a therapeutic target for neuroinflammatory pathologies. Considering the encouraging data obtained so far, clinical trials are warranted to demonstrate the effectiveness and potential use in the clinical practice of STAT inhibitors to treat inflammation-associated neurodegenerative pathologies.