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Risk promoting effects are different on each island, but obscured by meta-analysis or GWAS data from both islands, unless partitioned by different contributory factors. In Alzheimer's disease, the foxes appear to be herpes, borrelia or chlamydial infection, hypercholesterolemia, hyperhomocysteinaemia, diabetes, cerebral hypoperfusion, oestrogen depletion, or vitamin A deficiency, all of which promote beta-amyloid deposition in animal models\u2014without the aid of gene variants. All relate to risk factors and subsets of susceptibility genes, which condition their effects. All are less prevalent in convents, where nuns appear less susceptible to the ravages of ageing. Antagonism of the antimicrobial properties of beta-amyloid by Abeta autoantibodies in the ageing population, likely generated by antibodies raised to beta-amyloid\/pathogen protein homologues, may play a role in this scenario. These agents are treatable by diet and drugs, vitamin supplementation, pathogen detection and elimination, and autoantibody removal, although again, the beneficial effects of individual treatments may be tempered by genes and environment.<\/jats:p>","DOI":"10.5402\/2011\/394678","type":"journal-article","created":{"date-parts":[[2011,7,12]],"date-time":"2011-07-12T21:30:17Z","timestamp":1310506217000},"page":"1-29","source":"Crossref","is-referenced-by-count":8,"title":["The Fox and the Rabbits\u2014Environmental Variables and Population Genetics (1) Replication Problems in Association Studies and the Untapped Power of GWAS (2) Vitamin A Deficiency, Herpes Simplex Reactivation and Other Causes of Alzheimer's Disease"],"prefix":"10.5402","volume":"2011","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1368-4205","authenticated-orcid":true,"given":"C. 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