More than 10 million people worldwide suffer from cancer each year. Although the incidence of Alzheimer’s disease is not as good as that of cancer, there are more than 40 million patients worldwide. One disease causes the patient to die from the malignant proliferation of cells, while the other causes the death of neurons in the brain of patients.
In 1971, Richard Nixon, the president of the United States, signed the National Cancer Act to create a national cancer research project. Over the past 40 years, the field of cancer treatment has undergone great changes. Whether it is surgery, radiotherapy and chemotherapy, targeted therapy or immunotherapy, the choice of treatment options for cancer patients is increasing. The reduction in the mortality rate of multiple cancers and the increase in death rates are at the same time our deeper understanding of the disease, both at the molecular and overall levels. In the past few decades, we have not found any drugs that can slow the progression of Alzheimer’s disease. What caused our failure?
Last year, Axovant announced the failure of Phase 5 clinical trials of its 5-HT6 receptor antagonist Intepirdine. But this result will not be surprising. The Intepirdine obtained by Axovant from GSK is not like a clinical trial drug, but more like a tool to facilitate financing.
Maybe Vivek Ramaswamy really believes that clinical trials are likely to succeed. However, if other similar drugs have failed, and if the drug’s previous R&D has failed, what is the probability of doing another clinical success? If you invest this money in other projects for the development of new drugs for Alzheimer’s disease, you may be able to obtain more valuable output.
Whether it is the case of Solanezumab, or Intepirdine, or other drugs, after a clinical trial has failed, it is always possible to find some seemingly reasonable explanations for failures and propose improvement strategies, such as combining Aricept, such as changing doses, recruiting mild patients. Recruiting very early patients (Prodromal Alzheimer’s).
With the unlimited resources, I believe most people will choose to conduct follow-up studies. However, when time and money are limited, and there has been a huge investment in the previous period, on the other hand, when the huge market of products may bring extremely high profit after the listing, after the failure of the clinical trial is to stop the project or improve the strategy to continue the next clinical trial, It should be a test of the decision-making capabilities of corporate management.
However, the uncertainty of these clinical trial decisions is due to the lack of understanding of the disease. This is not only because we lack a reasonable animal model and lack of research tools, but also because of the complexity of our brains.
For the first time in Alois to report the case of Auguste, our understanding of the disease was still superficial after Kraepelin first used the term Alzheimer’s disease for more than a hundred years. In the past 100 years, we have proposed the amyloid cascade hypothesis, proposed the APOE4 hypothesis, put forward the Tau protein hypothesis, passed in vitro experiments, animal experiments, numerous clinical trials, but so far we still can not clearly Explain the mechanism of the disease.
Is starch protein the cause of disease? Perhaps this will still be one of the problems that most trouble us in the coming years.
Is the amyloid hypothesis falsified? Can a drug based on the Tau protein hypothesis be successful? Can we find a therapy that targets APOE4 and microglia? I don’t know the answer.
In distant Colombia, Miguel, 47, was diagnosed with Alzheimer’s disease years ago. His father died of the disease many years ago. Two of his family’s brothers and sisters were also diagnosed with the disease. His two sisters participated in the preventive clinical trial of crenezumab. Miguel’s brother asked Lopera, the doctor in charge of the clinical trial. Did we soon have treatment for Miguel?
Maybe it is.