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Abstract
Despite major strides in personalized genomics, it remains poorly understood why neurodegenerative diseases occur in only a fraction of individuals with a genetic predisposition and conversely, why individuals with no genetic risk of a disorder develop one. Chronic diseases like Alzheimer's, Parkinson's, and Multiple sclerosis are speculated to result from a combination of genetic and environmental factors, a concept commonly referred to as the “multiple hit hypothesis.” A number of bacterial infections have been linked to increased risk of neurodegeneration, and in some cases, clearance of bacterial pathogens has been correlated with amelioration of central nervous system (CNS) deficits. Additionally, mutations in several genes known to contribute to CNS disorders like Parkinson's Disease have repeatedly been implicated in susceptibility to intracellular bacterial infection. Recent data has begun to demonstrate roles for these genes (PARK2, PINK1, and LRRK2) in modulating innate immune outcomes, suggesting that immune dysregulation may play an even more important role in neurodegeneration than previously appreciated. This review will broadly explore the connections between bacterial infection, immune dysregulation, and CNS disorders. Understanding this interplay and how bacterial pathogenesis contributes to the “multiple-hit hypothesis” of neurodegeneration will be crucial to develop therapeutics to effectively treat both neurodegeneration and infection.
Highlights
An estimated 50 million people suffer from dementia/Alzheimer’s Disease (AD), 7– 10 million from Parkinson’s Disease (PD), and over 2 million from Multiple sclerosis (MS)
A recent study that investigated “infection burden” in a cohort of PD patients and healthy controls measured antibody titers for a number of infections that have been associated with neurodegeneration including cytomegalovirus (CMV), Epstein Barr virus (EBV), herpes simplex virus (HSV-1), Borrelia burgdorferi, Chlamydia pneumoniae, and Helicobacter pylori (Bu et al, 2015)
A study of patients in Denmark reported that patients who had been treated for H. pylori infection were at increased risk for developing PD (45% for H. pylori-eradication drugs and 23% for proton-pump inhibitors) (Nielsen et al, 2012), suggesting chronic H. pylori infection and/or gastritis precede PD symptoms
Summary
An estimated 50 million people suffer from dementia/Alzheimer’s Disease (AD), 7– 10 million from Parkinson’s Disease (PD), and over 2 million from Multiple sclerosis (MS). A recent study that investigated “infection burden” in a cohort of PD patients and healthy controls measured antibody titers for a number of infections that have been associated with neurodegeneration including cytomegalovirus (CMV), Epstein Barr virus (EBV), herpes simplex virus (HSV-1), Borrelia burgdorferi, Chlamydia pneumoniae, and Helicobacter pylori (Bu et al, 2015). They reported that PD patients were statistically more likely to have been exposed to multiple pathogens relative to healthy controls. As the links between PD and mycobacterial infections have been investigated with some mechanistic detail, we will explore the evidence that supports the “multiple-hit hypothesis” for PD
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