20220404_063517

1) PLEASE READ THIS ENTIRE THREAD. IT IS URGENT.Building on all recent work. By far my most important synthesis:A NEW KIND OF CANCER: THE MARRIAGE OF ONCOGENESIS AND PRIONOPATHYTHE PROGRESSIVE DESTRUCTION OF TISSUE AND ORGANS BY THE AMYLOIDOGENIC AND OLIGOMERIC PROPERTIES OF https://t.co/pXKEJgMwbI2) THE SARS-CoV-2 SPIKE PROTEINIt has been proposed that Alzheimer's disease might be a 'whole body' problem, as amyloid-beta can travel, cancer-like, to brain from other parts of body. Normal mice that had been joined (via bloodstreams) to genetically modified partners for a3) year "contracted" Alzheimer's disease. The researcher song says the amyloid-beta traveled from the genetically-modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.Not only did the normal mice develop plaques, but also 4) pathology similar to "TANGLES" -- twisted protein strands that form inside brain cells (please note, per image, this is PRECISELY what the Spike Protein induces), disrupting their function and eventually killing them from the inside-out. Other signs of Alzheimer's-like damage5) included brain cell degeneration, inflammation and microbleeds. In addition, the ability to transmit electrical signals involved in learning and memory -- a sign of a healthy brain -- was impaired, even in mice that had been joined for just four months.Besides the brain,6) amyloid-beta is produced in blood platelets, blood vessels and muscles, and its precursor protein is found in several other organs. But until these experiments, it was unclear if amyloid-beta from outside the brain could contribute to Alzheimer's disease.Which brings us to7) the Fibrils that the Spike Protein is inducing. Studies of nerve biopsy or cardiac autopsy specimens from patients with ATTR and AL amyloidoses show atrophy of cells near amyloid fibril aggregates. In addition to the stress or toxicity attributable to amyloid fibrils8) themselves, the toxicity of non-fibrillar states of amyloidogenic proteins, PARTICULARLY OLIGOMERS, may also participate in the mechanisms of tissue damage.By the way. Who discovered this? Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, THIRD9) MILITARY MEDICAL UNIVERSITY, Chongqing, China.The proposed therapeutics to deal with this pathology sound quite familiar: (1) reducing or preventing the production of causative proteins; (2) preventing the causative proteins from participating in the process of amyloid fibril10) formation; and/or (3) eliminating already-deposited amyloid fibrils.And this is what is MOST ALARMING and should cause the world to go FULL IMMEDIATE STOP ON ALL SPIKE PROTEIN THERAPIES. PLEASE READ (1) AGAIN!(1)REDUCING OR PREVENTING THE PRODUCTION OF CAUSITIVE PROTEINS.11) We need to make ourselves well, before we make ourselves ever more ill.https://t.co/og4QxKcA4qhttps://t.co/XOngMX9zii’https://t.co/Ql2m6p7umThttps://t.co/w8Srn4a56Phttps://t.co/4jvH3cOjBgWC