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Semorinenab does not reduce Clinical Decline in Alzheimer's Disease

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Clinical trial shows semorinenab is ineffective in slowing Alzheimer's disease

A clinical trial was conducted to evaluate the safety and effectiveness of a drug called semorinemab in people with prodromal to mild Alzheimer's disease. This drug is a type of antibody that targets a protein called tau, which is involved in the development of Alzheimer's disease. The goal of this trial was to determine if semorinemab could slow down or stop the progression of Alzheimer's disease in its early stages.

Clinical Trial

The trial included 457 participants from North America, Europe, and Australia. The participants were between 50 and 80 years old, had prodromal to mild Alzheimer's disease, and had confirmed beta-amyloid pathology. Beta-amyloid is another protein that accumulates in the brains of people with Alzheimer's disease.

During the 73-week study period, the participants received either semorinemab or a placebo. The participants in the semorinemab group received either a low dose (1500 mg), a medium dose (4500 mg), or a high dose (8100 mg) of the drug. The drug was given to the participants through an intravenous infusion every two weeks for the first three infusions and every four weeks thereafter.

The primary goal of the trial was to see if semorinemab could slow down the progression of Alzheimer's disease. The researchers looked at two main things: changes in the Clinical Dementia Rating–Sum of Boxes (CDR-SB) score and changes in the amount of tau in the brain, as measured by a special imaging test called [18F]GTP1 tau positron emission tomography.

Results

Unfortunately, the results of the trial were disappointing. The researchers found that the participants who received semorinemab did not show any significant difference in CDR-SB scores or tau accumulation compared to those who received the placebo. This means that semorinemab did not slow down the progression of Alzheimer's disease in these participants.

However, the researchers did find that semorinemab was generally safe and well-tolerated by the participants. The participants who received semorinemab did not experience any more side effects than those who received the placebo. This is important information because it means that semorinemab may be a safe treatment option for people with Alzheimer's disease in the future.

Overall, this trial suggests that targeting tau with semorinemab may not be an effective way to treat Alzheimer's disease. However, it is important to note that this trial only included people with prodromal to mild Alzheimer's disease. It is possible that semorinemab may be more effective in people with more advanced stages of the disease or in combination with other treatments.

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Conclusion

This clinical trial did not show any significant benefits of semorinemab in slowing down the progression of Alzheimer's disease in people with prodromal to mild forms of the disease. However, the drug was found to be safe and well-tolerated by the participants. More studies are needed to determine if semorinemab may be effective in treating Alzheimer's disease in other stages or in combination with other treatments.

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JAMA Network, Jun-13-22



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This content is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of such advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. CenTrial Data Ltd. does not take responsibility for possible health consequences of any person or persons reading or following the information in this educational content. Treatments and clinical trials mentioned may not be appropriate or available for all trial participants. Outcomes from treatments and clinical trials may vary from person to person. Consult with your doctor as to whether a clinical trial is a suitable option for your condition. Assistance from generative AI tools may have been used in writing this article.