Lääketiede huijausta: runsaudenpula löydetyistä mikrobeista kroonisissa sairauksissa - silti fokus pyöreä nolla näihin

Role of Microbes in the Development of Alzheimer's Disease: State of the Art –An International Symposium Presented at the 2017 IAGG Congress in San Francisco

-Prof. Itzhaki presented her work on the role of viruses, specically HSV-1, in the pathogenesis of AD. She maintains that although it is true that most people harbor HSV-1 infection, either latent or active, nonetheless aspects of herpes infection can play a role in the pathogenesis of AD, based on extensive experimental evidence from AD brains and infected cell cultures.

-Dr. Miklossy presented research on the high prevalence of bacterial infections that correlate with AD, specically spirochete infections, which have been known for a century to be a signicant cause of dementia (e.g., in syphilis). She demonstrated how spirochetes drive senile plaque formation, which are in fact biofilms

-Prof. Balin then described the involvement of brain tissue infection by the Chlamydia pneumoniae bacterium, with its potential to use the innate immune system in its spread, and its initiation of tissue damage characteristic of AD

-Prof. Fülöp described the role of AD-associated amyloid beta (Aβ) peptide as an antibacterial, antifungal and antiviral innate immune effector produced in reaction to microorganisms that attack the brain

-Prof. Barron put forward the novel hypothesis that, according to her experiments, there is strong sequence-specic binding between the AD-associated Aβ and another ubiquitous and important human innate immune effector, the cathelicidin peptide LL-37. Given this binding, LL-37 expression in the brain will decrease Aβ deposition via formation of non-toxic, soluble Aβ/LL-37 complexes. Therefore, a chronic underexpression of LL-37 could be the factor that simultaneously permits chronic infections in brain tissue and allows for pathological accumulation of Aβ.

Helppolukuista tekstiä, joka osoittaa kiistatta, että Alzheimerin tauti johtuu mikrobeista. Sekä on saatu uskottavin selitys koskaan siitä mitä Alzheimerin taudissa näkyvät amyloidiplakit ovat ja mistä ne tulevat.

Lääkefirmat ja lääkärit ovat silti kuin muissa maailmoissa, ja eivät ymmärrä asiaa miltään osin. Alzheimerin tautiin kehityt lääkkeet eivät auta mitään - ja se ei ole ihme, kun lääkkeet eivät ole kehitelty infektioiden hoitoon. Tilanne on tietenkin aivan sama muissakin kroonisissa sairauksissa. Iso puhallus.