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. 2015 Mar;5(1):177.
doi: 10.4172/2161-0460.1000177.

Microbial Sources of Amyloid and Relevance to Amyloidogenesis and Alzheimer's Disease (AD)

Y Zhao  1 , P Dua  2 , W J Lukiw  3
Affiliations

Microbial Sources of Amyloid and Relevance to Amyloidogenesis and Alzheimer's Disease (AD)

Y Zhao et al. J Alzheimers Dis Parkinsonism. 2015 Mar.

Abstract

Since the inception of the human microbiome project (HMP) by the US National Institutes of Health (NIH) in 2007 there has been a keen resurgence in our recognition of the human microbiome and its contribution to development, immunity, neurophysiology, metabolic and nutritive support to central nervous system (CNS) health and disease. What is not generally appreciated is that (i) the ~1014 microbial cells that comprise the human microbiome outnumber human host cells by approximately one hundred-to-one; (ii) together the microbial genes of the microbiome outnumber human host genes by about one hundred-and-fifty to one; (iii) collectively these microbes constitute the largest 'diffuse organ system' in the human body, more metabolically active than the liver; strongly influencing host nutritive-, innate-immune, neuroinflammatory-, neuromodulatory- and neurotransmission-functions; and (iv) that these microbes actively secrete highly complex, immunogenic mixtures of lipopolysaccharide (LPS) and amyloid from their outer membranes into their immediate environment. While secreted LPS and amyloids are generally quite soluble as monomers over time they form into highly insoluble fibrous protein aggregates that are implicated in the progressive degenerative neuropathology of several common, age-related disorders of the human CNS including Alzheimer's disease (AD). This general commentary-perspective paper will highlight some recent findings on microbial-derived secreted LPS and amyloids and the potential contribution of these neurotoxic and proinflammatory microbial exudates to age-related inflammatory amyloidogenesis and neurodegeneration, with specific reference to AD wherever possible.

Keywords: Alzheimer’s disease (AD); Beta amyloid precursor protein (βAPP); Congo Red (CR); Curli fibers; Hologenome; Inflammation; Innate-immunity; Senile (amyloid) plaques (SP); Toll receptor type 2 (TLR2).

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Figures

Figure 1
Figure 1
Potential contribution of gastrointestinal (GI) tract microbiome-derived lipopolysaccharide (LPS) and amyloids to systemic and central nervous system (CNS) amyloid burden
See this image and copyright information in PMC

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