Researchers have recently discovered an enzyme and a biochemical signaling pathway that they believe will lead to the discovery of drugs that inhibit beta-amyloid peptide production, which has long been held as the chief culprits of Alzheimer's disease.
Alzheimer's disease is characterized by accumulation of beta-amyloids and tau fragments, as well as loss of brain neurons. The FDA has not yet approved any drugs that can effectively prevent Alzheimer's disease.
After screening more than 75,000 small molecules, researchers from the Boston University School of Medicine (BUSM) and Boston University found a small molecule that inhibits the production of beta-amyloid in cell culture. "But more importantly, we have discovered the targets of these molecules, an enzyme and a biochemical signaling pathway, and we can reduce amyloid production by inhibiting this pathway." Dr. Cormela Abraham, professor of biochemistry at BUSM, co-author of the study said. Researchers say that the inhibitor of this pathway is also an anticancer drug, which is another example of the intersection of cancer and neurodegenerative diseases.
Researchers are optimistic that their research provides a new research path to delay or even prevent beta-amyloid formation. “We are in desperate need of drugs that can treat or even prevent Alzheimer's disease. We need further research to improve our small molecules, which will help produce new drug that can help treat millions of people who are at the risk of Alzheimer's disease.”
While there is no effective drug treatment for Alzheimer's, a new study has confirmed that physical exercise may be another option for people with Alzheimer's disease. Researchers from the Massachusetts General Hospital (MGH) found that neurogenesis in the brain structure that encodes memory—inducing the production of new neurons—can improve the Alzheimer’s cognitive function in a mouse model. Their research suggests that these beneficial effects on cognition can be disrupted by the harmful inflammatory environment present in the brains of Alzheimer's patients, and physical exercise can “clean up” the inflammatory environment, allowing new neurons to survive and improve the perception of a mouse model of Alzheimer's disease.
According to Dr. Rudolph Tanzi, the researcher of this study, they have confirmed in their study that physical exercise is perhaps one of the best ways to initiate neurogenesis. By identifying the molecular and genetic events involved, it has been determined as to how to simulate the beneficial effects of physical exercise through gene therapy and drugs.
- Dr. Se Hoon Choi of the Massachusetts General Hospital, also the first author of the paper, commented that “although we have not been able to achieve the same results safely on patients so far, we have determined how to develop proteins and gene targets with the same function in the future."