Prevention against Morbus Alzheimer’s disease is provided by Nervenzellen, which uses the best proteins in the treatment of Alzheimer’s disease. Bereits bei Alzheimer-Patientin, Auguste Deter, konnten post mortem Protein-Plaques and -Fibrillen im Gehirn detektiert werden.

Fibrils in neurons are best suited to healthy Tau protein, which is normal with microtubes of fibers in associated nerves. In the Erkrankungsfall kommt es zur Hyperphosphorylierung des Tau-Proteins et zur Konformationsänderung, was schließlich zu den beobachteten Fibrillen et Knäueln führt.

The plaques are made up of the amyloid beta (Aβ) peptide, which makes up the part of the amyloid precursor proteins (APP). APP is a transmembrane glycoprotein that is produced by the enzymes β and γ-sekretase. It contains Aβ-Peptide, which contains Aβ₄₀ and Aβ₄₂ The characteristics of pathogenicity are the same. The hydrophobic C-Terminus of Aβ₄₂ Sorgt für die Konformationsänderung des Proteins et die Aggregatbildung. Aggregated Aβ peptides are injected under underestimated conditions, such as the development process of nervous tissues and oxidative stress in cells, overnutrition of neurons. The war of things is also natural: The losses of amyloid plaques are reduced, the Absterben of the nerves are reduced and therefore the Fortschreiten der Erkrankung stops werden. Hier könnten Antikörper eingesetzt werden.