As a degenerative disease of the nervous system, patients with Alzheimer’s disease may experience memory loss, language problems, unresponsiveness, lostness, and abnormal mental behavior, leading to cognitive impairment and intellectual disability. For a long time, people have been expecting to prevent Alzheimer’s disease early by developing vaccines. In recent years, scientists seem to be approaching the end of victory, and some good news came from time to time.
Alzheimer’s disease is a neurodegenerative disease characterized by the gradual deposition of extracellular β-amyloid (Aβ) in the brain to form senile plaques and intracellular Tau protein hyperphosphorylation to form neurofibrillary tangles.Scientific research has found that Alzheimer’s disease is associated with aggregation and deposition of Aβ or Tau protein, and therefore, it has been the world’s Alz through the active (vaccine) and passive (antibody) immunosuppression or clearance of Aβ or Tau aggregation and deposition. Hotspots and key directions in the development of drug prevention and treatment for Haimo disease.
Recently, the results of the New Mexico State University (UNM) research, which was recently heated by the Internet, actually developed the animal model of frontotemporal dementia (FTD), rTg4510, which can alleviate the pathology of pure Tau protein aggregation. The researchers used virus-like particles (VLPs) to design a new vaccine. The experiment found that when the new vaccine was injected into the experimental mice, the mice produced antibodies that cleared the tau protein from the brain of the rats. A reaction lasted for several months.
However, the animal model used in the study was not an animal model of Alzheimer’s disease. And even if it achieves a certain effect on animal models, it does not mean that it will work equally well in humans.
The reporter learned that both Aβ vaccine and Tau vaccine are faced with the same paralysis: they may show good results in animal models, but once they enter the human clinical trial, they will lose the sand and can not show the same effect.
The reason may be related to the complexity of Alzheimer’s disease. Compared with the experimental transgenic animal model, the pathogenesis and pathological manifestations of human patients are more complicated.
Although this new network of vaccines can reduce the Tau load and improve the cognitive ability of the experimental mice, it is not a true “Alzheimer’s disease vaccine.” US researchers also admitted in an interview with local media that the successful development of the human Alzheimer’s disease vaccine “may take at least another decade.”