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A Novel Approach to the Treatment and Prevention of Alzheimer’s Disease Based on the Pathology and Microbiology
Journal of Alzheimer’s Disease ( IF 4 ) Pub Date : 2021-09-14 , DOI: 10.3233/jad-210429
Herbert B Allen 1, 2, 3
Affiliation  

Abstract

Utilizing the pathology and microbiology found in tissue from patients with documented Alzheimer’s disease (AD), the pathogenesis of this fateful disorder has been made clear. Borrelia burgdorferi and Treponema denticola spirochetes enter the brain, mostly via neuronal pathways and the entorhinal circulation. These organisms easily pass through the blood-brain barrier and have an affinity for neural tissue. Once in the brain, the spirochetes make intra- and extracellular biofilms, and it is the biofilms that create the pathology. Specifically, it is the intracellular biofilms that are ultimately responsible for neurofibrillary tangles and dendritic disintegration. The extracellular biofilms are responsible for the inflammation that initially is generated by the first responder, Toll-like receptor 2. The hypothesis that arises from this work is two-pronged: one is related to prevention; the other to treatment. Regarding prevention, it is very likely possible that AD could be prevented by periodic administration of penicillin (PCN), which would kill the spirochetes before they made biofilms; this would prevent the disease and would not allow any of the above deleterious changes generated by the biofilms to occur. As regards treatment, it may be possible to slow or prevent further decline in early AD by administration of PCN together with a biofilm disperser. The disperser would disrupt the biofilm coating and enable the PCN to kill the spirochetes. This protocol could be administered in a trial with the control arm utilizing the current treatment. The progress of the treatment could be evaluated by one of the current blood tests that is semi-quantitative. The specific protocols are listed.



中文翻译:

基于病理学和微生物学的阿尔茨海默病治疗和预防新方法

摘要

利用在有记录的阿尔茨海默病 (AD) 患者组织中发现的病理学和微生物学,已经明确了这种致命疾病的发病机制。伯氏疏螺旋体齿状密螺旋体螺旋体主要通过神经通路和内嗅循环进入大脑。这些生物很容易穿过血脑屏障,对神经组织有亲和力。一旦进入大脑,螺旋体就会形成细胞内和细胞外的生物膜,正是这些生物膜产生了病理。具体来说,是细胞内生物膜最终导致神经原纤维缠结和树突崩解。细胞外生物膜负责最初由第一反应者 Toll 样受体 2 产生的炎症。这项工作产生的假设有两个方面:一个与预防有关;另一个与预防有关。另一个来治疗。关于预防,很可能通过定期服用青霉素 (PCN) 来预防 AD,这将在螺旋体形成生物膜之前杀死它们;这将预防疾病并且不会允许由生物膜产生的任何上述有害变化发生。在治疗方面,通过将 PCN 与生物膜分散剂一起给药,可以减缓或防止早期 AD 的进一步下降。分散器会破坏生物膜涂层并使 PCN 能够杀死螺旋体。该方案可以在使用当前治疗的对照组的试验中进行。可以通过目前半定量的血液测试之一来评估治疗的进展。列出了具体的协议。通过将 PCN 与生物膜分散剂一起给药,可以减缓或防止早期 AD 的进一步下降。分散器会破坏生物膜涂层并使 PCN 能够杀死螺旋体。该方案可以在使用当前治疗的对照组的试验中进行。可以通过目前半定量的血液测试之一来评估治疗的进展。列出了具体的协议。通过将 PCN 与生物膜分散剂一起给药,可以减缓或防止早期 AD 的进一步下降。分散器会破坏生物膜涂层并使 PCN 能够杀死螺旋体。该方案可以在使用当前治疗的对照组的试验中进行。可以通过目前半定量的血液测试之一来评估治疗的进展。列出了具体的协议。可以通过目前半定量的血液测试之一来评估治疗的进展。列出了具体的协议。可以通过目前半定量的血液测试之一来评估治疗的进展。列出了具体的协议。

更新日期:2021-09-15
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