Microbial Sources of Amyloid and Relevance to Amyloidogenesis and AlzheimerÃ¢ÂÂs Disease (AD)
- Corresponding Author:
- Walter J Lukiw
Professor of Neuroscience
Neurology and Ophthalmology Bollinger Professor of Alzheimerâ€™s disease
LSU Neuroscience Center of Excellence
Louisiana State University Health Sciences Center2020 Gravier Street, Suite 904
E-mail: [email protected]
Received date: December 14, 2014; Accepted date: January 05, 2015; Published date: January 15, 2015
Citation: Lukiw WJ, Zhao Y and Dua P (2015) Microbial Sources of Amyloid and Relevance to Amyloidogenesis and Alzheimerâ€™s Disease (AD). J Alzheimers Dis Parkinsonism 5:177. doi:10.4172/2161-0460.1000177
Copyright: © 2015 Walter J. Lukiw et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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 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.