Medication Did Not Decrease Cognitive Loss in Patients with Alzheimer Disease

Bottom Line: The use of the drug idalopirdine for six months did not improve or reduce the loss of cognition for patients with mild to moderate Alzheimer disease.

Why The Research Is Interesting: Two phase 2 trials have suggested that a certain type of drug, a selective 5-hydroxytryptamine-6 receptor antagonist, such as idalopirdine, may improve cognition in Alzheimer disease when added with another type of drug, cholinesterase inhibitors.

Who: 2,525 patients ages 50 years or older with mild to moderate Alzheimer disease

When: October 2013 to January 2017

What (Study Measures): Changes in measures of cognition from study entry to 24 weeks.

How (Study Design): Three randomized clinical trials, in which patients were assigned to receive idalopirdine or placebo added to a cholinesterase inhibitor. Randomized clinical trials allow for the strongest inferences to be made about the true effect of an intervention such as a medication or a procedure.

Authors: Alireza Atri, M.D., Ph.D., of California Pacific Medical Center, San Francisco, and Brigham and Women’s Hospital/Harvard Medical School, Boston, and coauthors

Results and Study Conclusions: Six months of idalopirdine treatment added to cholinesterase inhibitor therapy did not improve cognition or decrease cognitive loss in patients with mild to moderate Alzheimer disease. These findings do not support the use of idalopirdine for the treatment of Alzheimer disease.

Study Limitations: There was no requirement for evidence of Alzheimer disease biomarker positivity for inclusion in a trial, which may have allowed some patients to be included without having Alzheimer disease pathology.

Related material: The following related elements also are available on the For The Media website:

  • The editorial, Lack of Benefit With Idalopirdine for Alzheimer Disease,” by David A. Bennett, M.D., Rush University Medical Center, Chicago.

For more details and to read the full study, please visit the For The Media website.