With regards to LOAD, Cpn has been studied as a possible etiologic agent [1,2] and supporting evidence for Cpn in the etiopathogenesis of AD was provided by a study by Little et al. 2004 which revealed amyloid deposits resembling plaques found in AD brains in the brains of non-transgenic BALB/c mice following intranasal infection with Cpn [42]. This evidence concerns the gene CPN1 and Alzheimer disease.