Purdey Mark
High Barn Farm, Elworthy, Taunton, Somerset TA4 3PX, UK.
Med Hypotheses. 2005;65(3):448-77. doi: 10.1016/j.mehy.2005.03.018.
This paper exposes the flaws in the conventional consensus on the origins of transmissible spongiform encephalopathies (TSEs) which decrees that the protein-only misfolded 'prion' represents the primary aetiological transmissible agent, and then reviews/presents the emerging data which indicates that environmental exposure to metal microcrystal pollutants (sourced from munitions, etc.) represents the heat resistant, transmissible nucleating agents which seed the metal-prion protein (PrP)-ferritin fibril crystals that cause TSE. Fresh analytical data is presented on the levels of metals in ecosystems which support populations affected by clusters of variant Creutzfeldt-Jacob disease (vCJD), sporadic/familial CJD, and the scrapie types of TSE that have emerged in the UK, Sicily, Sardinia, Calabria and Japan. This data further substantiates the abnormal geochemical template (e.g., elevated strontium (Sr), barium (Ba) and silver (Ag)) which was observed as a common hallmark of the TSE cluster ecosystems across North America, thereby supporting the hypothesis that these microcrystals serve as the piezoelectrion nucleators which seed the growth/multireplication of the aberrant metal-PrP-ferritin fibril features which characterise the neuropathology of the TSE diseased brain. A secondary pathogenic mechanism entails the inactivation of the sulphated proteoglycans which normally regulate the mineralisation process. This can be induced by a rogue metal mediated chelation of free sulphur, or by contamination with organo-sulphur pollutants that substitute at natural sulphur bonds, or via a mutation to the S-proteoglycan cell line; thereby enabling the aberrant overgrowth of rogue fibril crystal formations that possess a piezoelectric capacity which compromises the ability of the contaminated individual to process incoming acoustic/tactile pressure waves in the normal way. The crystals transduce incoming sonic energy into electrical energy, which, in turn, generates magnetic fields on the crystal surfaces that initiate chain reactions of free radical mediated spongiform neurodegeneration. Metal microcrystal nucleating agents provide a group of plausible aetiological candidates that explain the unique properties of the TSE causal agent - such as heat resistance, transmissibility, etc. - which the protein-only prion model fails to fulfill. This paper also discusses the possible nutritional measures that could best be adopted by populations living in high risk TSE ecosystems; as a means of preventing the successful implantation of these rogue microcrystals and their consequent hypermineralisation of the soft tissues within the CNS.
本文揭示了关于传染性海绵状脑病（TSEs）起源的传统共识中的缺陷，该共识认为仅蛋白质错误折叠的“朊病毒”是主要的病因性传播因子，然后回顾/展示了新出现的数据，这些数据表明环境暴露于金属微晶污染物（源自弹药等）代表了耐热、可传播的成核剂，它们引发了导致TSE的金属 - 朊病毒蛋白（PrP） - 铁蛋白纤维晶体。给出了关于生态系统中金属水平的新分析数据，这些生态系统支持受变异型克雅氏病（vCJD）、散发性/家族性克雅氏病以及在英国、西西里岛、撒丁岛、卡拉布里亚和日本出现的TSE痒病类型影响的人群。这些数据进一步证实了异常地球化学模板（例如，锶（Sr）、钡（Ba）和银（Ag）升高），这在北美TSE聚集生态系统中被观察到是一个共同特征，从而支持了这样的假设，即这些微晶作为压电成核剂，引发了异常金属 - PrP - 铁蛋白纤维特征的生长/多重复制，这些特征是TSE病脑神经病理学的特征。第二种致病机制涉及通常调节矿化过程的硫酸化蛋白聚糖的失活。这可以由流氓金属介导的游离硫螯合、被取代天然硫键的有机硫污染物污染或通过S - 蛋白聚糖细胞系的突变诱导；从而使具有压电能力的流氓纤维晶体形成异常过度生长，这损害了受污染个体以正常方式处理传入声/触觉压力波的能力。这些晶体将传入的声能转换为电能，进而在晶体表面产生磁场，引发自由基介导的海绵状神经变性的连锁反应。金属微晶成核剂提供了一组合理的病因候选者，解释了TSE病原体的独特特性——如耐热性、可传播性等——这是仅蛋白质朊病毒模型无法满足的。本文还讨论了生活在高风险TSE生态系统中的人群可以最好地采用的可能营养措施；作为防止这些流氓微晶成功植入及其随后中枢神经系统内软组织过度矿化的一种手段。
