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Toward the end of his 1976 book entitled “Vitamin C and the Common Cold” Linus Pauling included an interesting chapter on “human biochemical individuality” that defined some important parameters on individual human genotypic versus phenotypic variation, based in part on studies from hemoglobin genetics (Pauling, 1976). That chapter provided theoretical calculations and novel insight on genomic diversity, discussing, that when any genetic characteristic is analyzed in a sampling of 100 human beings, wide ranges in values are invariably observed. The “normalcy” range was defined as that in which 95% of those “normal values” lie, while the remaining 5% are described as “abnormal.” Defining “normalcy” on a larger scale becomes a bit trickier however, and Pauling proposed that if we assume that 500 characters are independently inherited, then we can calculate that there is only a small chance, 10%, that one person in the entire global population would be normal (with respect to each of these 500 characters). If we assume that there are about 26,600 human genes available to be expressed in each cell and that each gene is responsible for at least one inherited trait or genetic function (a number that is probably vastly underestimated), in a global human population exceeding 7 billion it then becomes exceedingly difficult to define “human genetic normalcy.” These ideas form the basis for the evolving concept of “human genetic individuality” and our ongoing efforts to better understand the genotypic basis of human phenotypic diversity in both health and disease (Li et al., 2010; Raj et al., 2010; Lukiw, 2012a,b; Olson, 2012; this paper). More recently, large population studies have analyzed the contribution of variability in gene expression, including the impact of genetic mutations, to “human genetic normalcy,” “human genetic individuality,” phenotype, susceptibility to disease and related parameters that include the general redundancy in human gene expression that may directly impact the genetic evolution of the human species (Colangelo et al., 2002; Li et al., 2010; Zheng et al., 2011; Lukiw, 2012a,b; Ginsberg et al., 2012; Raj et al., 2012; Hulse and Cai, 2013). This “Opinion paper” addresses an observed variability in micro RNA (miRNA) abundance, speciation and complexity in Alzheimer's disease (AD), a common, progressive neurological disorder unique to the aging human brain whose incidence is approaching epidemic proportions (Alzheimer Association, 2013). Here we define miRNA abundance as how much of each individual miRNA species is present, miRNA speciation as what individual miRNA species are present, and miRNA complexity as the pattern of miRNA abundance and speciation representative of a particular physiological or pathophysiological state.

frontiers in cellular neuroscience

Variability in micro RNA (miRNA) abundance, speciation and complexity amongst different human populations and potential relevance to Alzheimer's disease (AD)