疫苗中神经毒素铝沉积大脑 是削弱人类思辨能力 易于统治的手段 阿尔茨海默病与老年痴呆 The deposition of neurotoxic aluminum in the brain through vaccines is a method to weaken human cognitive abilities, making it easier to govern. Alzheimer’s disease and dementia
I began my research on Alzheimer’s disease in the early 1990s. A role for aluminium in the aetiology of the disease had yet to be ascribed to quackery. This period of common sense science did not last as I explain later. During these thirty years or so I have witnessed many false dawns in the field of Alzheimer’s research and specifically treatment. One…我于 20 世纪 90 年代初开始研究阿尔茨海默病。 铝在该疾病病因学中的作用尚未被归咎于庸医。 正如我稍后解释的那样，这个常识科学时期并没有持续下去。 在这三十年左右的时间里，我目睹了阿尔茨海默病研究和特别是治疗领域的许多虚假曙光。 一…
In my previous musing I promised to explain why I came to the conclusion 'no aluminium, no Alzheimer's'. By 2017, when this paper was published, there was already a wealth of clinical and animal studies providing almost unequivocal evidence of aluminium as a cause of Alzheimer’s disease. Today it still raises a wry smile when I read research where treatment strategies for Alzheimer’s disease are tested in animal models where Alzheimer’s disease is induced by the injection of aluminium salts. Indeed animal studies continue to this day to recapitulate the role of aluminium in Alzheimer's disease. However, to this moment in time, mainstream media, Alzheimer’s charities and the governments of developed countries deny aluminium’s involvement in the disease and are quick to bring out the old chestnut that aluminium’s role in Alzheimer’s disease has been disproved, they like to say debunked, years ago. I knew that I had to play the detractors at their own game. Take an idea that most if not all of the Alzheimer’s mafia are happy to promote and turn this idea on its head by introducing aluminium into the (their) picture. The accepted idea I addressed being that early onset Alzheimer’s disease was a genetic form of the disease mediated through genes relating to the processing of the amyloid precursor protein. The latter being the parent protein of amyloid beta, the peptide that forms the senile plaques found in Alzheimer’s disease brain tissue. See the post below and other similar posts for further background on amyloid beta. 在我之前的沉思中，我承诺解释为什么我得出“没有铝，就没有阿尔茨海默病”的结论。 到 2017 年，当这篇论文发表时，已经有大量的临床和动物研究提供了几乎明确的证据，证明铝是导致阿尔茨海默病的原因。 今天，当我读到有关阿尔茨海默病治疗策略在动物模型中进行测试的研究时，我仍然会苦笑，在动物模型中，阿尔茨海默病是通过注射铝盐诱发的。 事实上，动物研究至今仍在继续，以概括铝在阿尔茨海默病中的作用。 然而，时至今日，主流媒体、阿尔茨海默氏症慈善机构和发达国家政府都否认铝与该疾病有关，并很快拿出了老生常谈的说法，即铝在阿尔茨海默氏症中的作用已被证明是错误的，他们喜欢说，几年前就已经被揭穿了。 我知道我必须与批评者玩他们自己的游戏。 假设大多数（如果不是全部）阿尔茨海默氏症黑手党都乐于通过在（他们的）照片中引入铝来宣传和扭转这一想法。 我提出的公认观点是，早发性阿尔茨海默氏病是一种通过与淀粉样前体蛋白加工相关的基因介导的疾病的遗传形式。 后者是β淀粉样蛋白的母体蛋白，β淀粉样蛋白是形成阿尔茨海默病脑组织中老年斑的肽。 有关淀粉样蛋白β的更多背景信息，请参阅下面的帖子和其他类似的帖子。
I reasoned with myself that if aluminium was absolutely the cause of Alzheimer’s disease, sometimes called sporadic disease, then it must also be the cause of early onset or familial Alzheimer’s disease (fAD). I set about locating a source of brain tissue from donors who died with a diagnosis of fAD. I found such tissue at the MRC London Neurodegenerative Diseases Brain Bank and collaborated with their chief neuropathologist Dr Andrew King who provided us with brain tissue from twelve donors who died with a diagnosis of fAD. The aluminium content of these brain tissues taken from donors with a confirmed diagnosis of fAD were little short of astonishing. They represented at that time some of the highest concentrations of aluminium ever recorded in human brain tissue. We concluded that such levels of neurotoxic aluminium were unlikely to be benign and would have contributed to both the onset and aggressive nature of Alzheimer’s disease in these donors. Later in our seminal study on aluminium in brain tissue in donors without neurodegenerative disease we showed that the concentrations of aluminium in fAD were significantly different (P=0.0020), much, much higher, to those without neurodegenerative or neurodevelopmental disease. This important research created no more than a murmur in the Alzheimer’s disease fraternity and even to the extent that organisations such as the Alzheimer’s Society warned their members against taking any notice of it. Not deterred I set about repeating the study with another recognised cohort of familial Alzheimer’s disease from Colombia. This population of individuals had already been the subject of myriad published studies and so implicating aluminium in their well-documented histories would prove difficult to ignore. Tissues were sent from the brain bank in Colombia and we measured their content of aluminium and carried out complementary aluminium-specific fluorescence to identify the location of aluminium. As with our previous study on fAD the results were remarkable and proved without any doubt that individuals who have died with a diagnosis of fAD have extremely high concentrations of aluminium in their brain tissues. The paper was accepted for publication in the Journal of Alzheimer’s Disease and the Editor-in-Chief, Professor George Perry, wrote a press release in which he described our paper as a landmark study in the field of Alzheimer’s disease. We also included in the paper some of the most remarkable images of the co-localisation of aluminium and amyloid beta ever witnessed, see example below. 我对自己推理，如果铝绝对是阿尔茨海默病（有时称为散发性疾病）的原因，那么它也一定是早发或家族性阿尔茨海默病 (fAD) 的原因。 我开始寻找死于 fAD 的捐赠者的脑组织来源。 我在 MRC 伦敦神经退行性疾病脑库中发现了这样的组织，并与他们的首席神经病理学家安德鲁·金博士合作，他为我们提供了 12 名死于 fAD 的捐赠者的脑组织。 这些从确诊为 fAD 的捐献者身上采集的脑组织中的铝含量几乎令人惊讶。 它们代表了当时人类脑组织中铝含量最高的记录。 我们得出的结论是，如此水平的神经毒性铝不太可能是良性的，并且会导致这些捐赠者阿尔茨海默病的发作和侵袭性。 后来，在我们对没有神经退行性疾病的捐献者脑组织中的铝进行的开创性研究中，我们发现，fAD 中的铝浓度与没有神经退行性疾病或神经发育疾病的捐献者相比显着不同（P=0.0020），而且要高得多。 这项重要的研究在阿尔茨海默病协会中只引起了一阵议论，甚至阿尔茨海默病协会等组织警告其成员不要对此给予任何关注。 我并没有被吓倒，开始对来自哥伦比亚的另一组公认的家族性阿尔茨海默病患者重复这项研究。 这群人已经成为无数已发表研究的主题，因此很难忽视铝与他们有据可查的历史的关系。 组织是从哥伦比亚的脑库送来的，我们测量了它们的铝含量，并进行了互补的铝特异性荧光以确定铝的位置。 与我们之前对 fAD 的研究一样，结果是显着的，并且毫无疑问地证明，死于 fAD 诊断的个体的脑组织中铝浓度极高。 这篇论文被《阿尔茨海默病杂志》接受发表，主编乔治·佩里教授撰写了一份新闻稿，他在新闻稿中将我们的论文描述为阿尔茨海默病领域的一项里程碑式的研究。 我们还在论文中收录了一些有史以来见证过的铝和淀粉样蛋白共定位的最引人注目的图像，请参见下面的示例。
疫苗中神经毒素铝沉积大脑 是削弱人类思辨能力 易于统治的手段 阿尔茨海默病与老年痴呆
The deposition of neurotoxic aluminum in the brain through vaccines is a method to weaken human cognitive abilities, making it easier to govern. Alzheimer’s disease and dementia
https://open.substack.com/pub/drchristopherexley/p/alzheimers-disease-is-caused-by-aluminium
I began my research on Alzheimer’s disease in the early 1990s. A role for aluminium in the aetiology of the disease had yet to be ascribed to quackery. This period of common sense science did not last as I explain later. During these thirty years or so I have witnessed many false dawns in the field of Alzheimer’s research and specifically treatment. One…我于 20 世纪 90 年代初开始研究阿尔茨海默病。 铝在该疾病病因学中的作用尚未被归咎于庸医。 正如我稍后解释的那样，这个常识科学时期并没有持续下去。 在这三十年左右的时间里，我目睹了阿尔茨海默病研究和特别是治疗领域的许多虚假曙光。 一…
In my previous musing I promised to explain why I came to the conclusion 'no aluminium, no Alzheimer's'. By 2017, when this paper was published, there was already a wealth of clinical and animal studies providing almost unequivocal evidence of aluminium as a cause of Alzheimer’s disease. Today it still raises a wry smile when I read research where treatment strategies for Alzheimer’s disease are tested in animal models where Alzheimer’s disease is induced by the injection of aluminium salts. Indeed animal studies continue to this day to recapitulate the role of aluminium in Alzheimer's disease. However, to this moment in time, mainstream media, Alzheimer’s charities and the governments of developed countries deny aluminium’s involvement in the disease and are quick to bring out the old chestnut that aluminium’s role in Alzheimer’s disease has been disproved, they like to say debunked, years ago.
I knew that I had to play the detractors at their own game. Take an idea that most if not all of the Alzheimer’s mafia are happy to promote and turn this idea on its head by introducing aluminium into the (their) picture. The accepted idea I addressed being that early onset Alzheimer’s disease was a genetic form of the disease mediated through genes relating to the processing of the amyloid precursor protein. The latter being the parent protein of amyloid beta, the peptide that forms the senile plaques found in Alzheimer’s disease brain tissue. See the post below and other similar posts for further background on amyloid beta. 在我之前的沉思中，我承诺解释为什么我得出“没有铝，就没有阿尔茨海默病”的结论。 到 2017 年，当这篇论文发表时，已经有大量的临床和动物研究提供了几乎明确的证据，证明铝是导致阿尔茨海默病的原因。 今天，当我读到有关阿尔茨海默病治疗策略在动物模型中进行测试的研究时，我仍然会苦笑，在动物模型中，阿尔茨海默病是通过注射铝盐诱发的。 事实上，动物研究至今仍在继续，以概括铝在阿尔茨海默病中的作用。 然而，时至今日，主流媒体、阿尔茨海默氏症慈善机构和发达国家政府都否认铝与该疾病有关，并很快拿出了老生常谈的说法，即铝在阿尔茨海默氏症中的作用已被证明是错误的，他们喜欢说，几年前就已经被揭穿了。
我知道我必须与批评者玩他们自己的游戏。 假设大多数（如果不是全部）阿尔茨海默氏症黑手党都乐于通过在（他们的）照片中引入铝来宣传和扭转这一想法。 我提出的公认观点是，早发性阿尔茨海默氏病是一种通过与淀粉样前体蛋白加工相关的基因介导的疾病的遗传形式。 后者是β淀粉样蛋白的母体蛋白，β淀粉样蛋白是形成阿尔茨海默病脑组织中老年斑的肽。 有关淀粉样蛋白β的更多背景信息，请参阅下面的帖子和其他类似的帖子。
I reasoned with myself that if aluminium was absolutely the cause of Alzheimer’s disease, sometimes called sporadic disease, then it must also be the cause of early onset or familial Alzheimer’s disease (fAD).
I set about locating a source of brain tissue from donors who died with a diagnosis of fAD. I found such tissue at the MRC London Neurodegenerative Diseases Brain Bank and collaborated with their chief neuropathologist Dr Andrew King who provided us with brain tissue from twelve donors who died with a diagnosis of fAD.
The aluminium content of these brain tissues taken from donors with a confirmed diagnosis of fAD were little short of astonishing. They represented at that time some of the highest concentrations of aluminium ever recorded in human brain tissue. We concluded that such levels of neurotoxic aluminium were unlikely to be benign and would have contributed to both the onset and aggressive nature of Alzheimer’s disease in these donors.
Later in our seminal study on aluminium in brain tissue in donors without neurodegenerative disease we showed that the concentrations of aluminium in fAD were significantly different (P=0.0020), much, much higher, to those without neurodegenerative or neurodevelopmental disease.
This important research created no more than a murmur in the Alzheimer’s disease fraternity and even to the extent that organisations such as the Alzheimer’s Society warned their members against taking any notice of it.
Not deterred I set about repeating the study with another recognised cohort of familial Alzheimer’s disease from Colombia. This population of individuals had already been the subject of myriad published studies and so implicating aluminium in their well-documented histories would prove difficult to ignore.
Tissues were sent from the brain bank in Colombia and we measured their content of aluminium and carried out complementary aluminium-specific fluorescence to identify the location of aluminium. As with our previous study on fAD the results were remarkable and proved without any doubt that individuals who have died with a diagnosis of fAD have extremely high concentrations of aluminium in their brain tissues. The paper was accepted for publication in the Journal of Alzheimer’s Disease and the Editor-in-Chief, Professor George Perry, wrote a press release in which he described our paper as a landmark study in the field of Alzheimer’s disease.
We also included in the paper some of the most remarkable images of the co-localisation of aluminium and amyloid beta ever witnessed, see example below. 我对自己推理，如果铝绝对是阿尔茨海默病（有时称为散发性疾病）的原因，那么它也一定是早发或家族性阿尔茨海默病 (fAD) 的原因。
我开始寻找死于 fAD 的捐赠者的脑组织来源。 我在 MRC 伦敦神经退行性疾病脑库中发现了这样的组织，并与他们的首席神经病理学家安德鲁·金博士合作，他为我们提供了 12 名死于 fAD 的捐赠者的脑组织。
这些从确诊为 fAD 的捐献者身上采集的脑组织中的铝含量几乎令人惊讶。 它们代表了当时人类脑组织中铝含量最高的记录。 我们得出的结论是，如此水平的神经毒性铝不太可能是良性的，并且会导致这些捐赠者阿尔茨海默病的发作和侵袭性。
后来，在我们对没有神经退行性疾病的捐献者脑组织中的铝进行的开创性研究中，我们发现，fAD 中的铝浓度与没有神经退行性疾病或神经发育疾病的捐献者相比显着不同（P=0.0020），而且要高得多。
这项重要的研究在阿尔茨海默病协会中只引起了一阵议论，甚至阿尔茨海默病协会等组织警告其成员不要对此给予任何关注。
我并没有被吓倒，开始对来自哥伦比亚的另一组公认的家族性阿尔茨海默病患者重复这项研究。 这群人已经成为无数已发表研究的主题，因此很难忽视铝与他们有据可查的历史的关系。
组织是从哥伦比亚的脑库送来的，我们测量了它们的铝含量，并进行了互补的铝特异性荧光以确定铝的位置。 与我们之前对 fAD 的研究一样，结果是显着的，并且毫无疑问地证明，死于 fAD 诊断的个体的脑组织中铝浓度极高。 这篇论文被《阿尔茨海默病杂志》接受发表，主编乔治·佩里教授撰写了一份新闻稿，他在新闻稿中将我们的论文描述为阿尔茨海默病领域的一项里程碑式的研究。
我们还在论文中收录了一些有史以来见证过的铝和淀粉样蛋白共定位的最引人注目的图像，请参见下面的示例。