Antiviral Treatment for Alzheimer's Disease Shows No Efficacy in Trials

In a landmark clinical trial led by researchers at Columbia University Vagelos College of Physicians and Surgeons, the antiviral medication valacyclovir, typically used for herpes simplex infections, has been found ineffective in slowing the progression of early-stage Alzheimer's disease. This study, which included 120 participants diagnosed with either early Alzheimer's or mild cognitive impairment, was presented at the Alzheimer's Association International Conference on July 29, 2025.

The notion that herpes infections may contribute to Alzheimer's has gained traction among some scientists, with previous studies suggesting a correlation between herpes simplex virus (HSV) infections and Alzheimer's pathology. In the United States, it is estimated that 60% to 70% of the population carries HSV, which can remain dormant in the nervous system and reactivate over time. Notably, some autopsy studies revealed that HSV1 DNA was frequently found alongside amyloid plaques in the brains of Alzheimer's patients.

Dr. D.P. Devanand, the trial's lead investigator and a professor of psychiatry and neurology at Columbia University, highlighted that earlier studies indicated a reduced risk of Alzheimer's among individuals treated for herpes infections. However, this clinical trial aimed to directly assess the efficacy of valacyclovir in altering cognitive decline associated with Alzheimer's.

Participants, with an average age of 71, were randomly assigned to receive either valacyclovir or a placebo for 18 months. Cognitive assessments and neuroimaging were conducted to evaluate changes in memory function, amyloid and tau deposits, and other structural brain changes. Contrary to expectations, the results indicated that those receiving the placebo performed slightly better on cognitive tests than those taking valacyclovir. Overall, there were no significant differences in cognitive decline or brain pathology between the two groups.

Dr. Devanand stated, "We were looking for a signal that the drug did better than the placebo, but there wasn't any in this study. Our trial suggests antivirals that target herpes are not effective in treating early Alzheimer's and cannot be recommended for such patients with evidence of prior HSV infection."

The implications of these findings are substantial. As researchers continue to explore potential therapeutic avenues for Alzheimer's disease, the failure of valacyclovir underscores the complexities involved in addressing this multifaceted condition. Future research may need to focus on other avenues, including long-term antiviral treatment following HSV infections, as prospective controlled trials on this topic have yet to be conducted.

In a broader context, the study contributes to the ongoing discourse about the links between viral infections and neurodegenerative diseases. While the connection between herpes simplex viruses and Alzheimer's disease remains an area of intrigue, it is clear that more rigorous research is necessary to elucidate these relationships and identify viable treatment options for Alzheimer’s patients. As the search for effective Alzheimer’s therapies continues, this trial serves as a reminder of the challenges inherent in finding solutions to such a complex and devastating disease.