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   Front Cell Neurosci. 2013; 7: 153.    
   Published online 2013 Sep 17. doi:  10.3389/fncel.2013.00153    
   PMCID: PMC3775450    
      
   Alzheimer's disease and the microbiome    
   Surjyadipta Bhattacharjee and Walter J. Lukiw*    
   Author information ► Article notes ► Copyright and License information ►    
   This article has been cited by other articles in PMC.    
      
   “Microbial colonization of mammals is an evolution-driven process that   
   modulates host physiology, many of which are associated with immunity and   
   nutrient intake”—Heijtz et al.(2011)    
      
   The recognition of the human microbiome (HM) as a substantial contributor to   
   nutrition, health and disease is a relatively recent one, and currently,   
   peer-reviewed studies linking alterations in microbiota to the etiopathology   
   of human disease are few.    
   Emerging studies indicate that the HM may contribute to the regulation of   
   multiple neuro-chemical and neuro-metabolic pathways through a complex series   
   of highly interactive and symbiotic host-microbiome signaling systems that   
   mechanistically    
   interconnect the gastrointestinal (GI) tract, skin, liver, and other organs   
   with the central nervous system (CNS). For example, the human GI tract,   
   containing 95% of the HM, harbors a genetically diverse microbial population   
   that plays major roles in    
   nutrition, digestion, neurotrophism, inflammation, growth, immunity and   
   protection against foreign pathogens (Forsythe et al., 2012; Collins et al.,   
   2013; Douglas-Escobar et al., 2013; see below). It has been estimated that   
   about 100 trillion bacteria    
   from up to 1000 distinct bacterial species co-inhabit the human GI tract,   
   albeit in different stoichiometries amongst individuals, and the varying   
   combinations and strains of bacterial species amongst human populations might   
   contribute, in part, to “   
   human-biochemical” or “genetic-individuality” and resistance to disease   
   (Aziz et al., 2013; Lukiw, 2013). Interestingly, HM participation in human   
   physiology may also help explain the genome-complexity conundrum—for example   
   why the 26,600 protein-   
   encoding transcripts in Homo sapiens are far fewer in number, than for   
   example, the rice genome (Oryza sativa; which has about 46,000 functional   
   genes). One thousand different strains of bacteria might be expected to   
   contribute up to 4 × 106 potential    
   mRNAs to the human transcriptome, thus making the human host-plus-microbiome   
   genetic complexity closer to 4,026,600 mRNA transcripts, and a clear   
   “winner” of human genetic complexity over that of rice and other species   
   (Venter et al., 2001; Foster    
   and McVey Neufeld, 2013; Lukiw, 2013). The very recent observation of   
   microbiome-derived small non-coding RNA (sncRNA) and micro RNA (miRNA)   
   translocation and signaling across endothelial barriers, between cells and   
   tissues, and even perhaps between    
   individual species indicates that human neurobiology may be significantly   
   impacted by the actions of HM-mediated sncRNA or miRNA trafficking, and the   
   integration of a cell, tissue or an entire organism into its local environment   
   (Zhao et al., 2006;    
   Alexandrov et al., 2012; Sarkies and Miska, 2013; Reijerkerk et al., 2013;   
   unpublished). This opinion paper encompasses what we know concerning the   
   contribution of the HM to neurological disease, with specific emphasis on   
   Alzheimer's disease (AD)    
   wherever possible.    
      
      
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