A new study demonstrated positive effects for CAD106, an active vaccine against Alzheimer's disease (AD), the most common cause of dementia.

Researchers at Karolinska Institutet (Stockholm, Sweden) conducted a phase 1 study in two centers in Sweden between August 2005, and March 2007. The researchers randomly allocated 31 patients into cohort one (24 patients to CAD106 treatment and 7 to placebo) and 27 patients into cohort two (22 patients to CAD106 treatment and 5 to placebo). Each patient received three subcutaneous injections. All patients, caregivers, and investigators were masked to treatment allocation throughout the study. The primary objectives were to assess the safety and tolerability of CAD106 and to identify the amyloid β (Aβ)-specific antibody response.

The results showed that 56 of 58 patients reported adverse events. In cohort one, nasopharyngitis was the most commonly reported adverse event (10 of 24 CAD106-treated patients). In cohort two, injection site erythema was the most commonly reported adverse event (14 of 22 CAD106-treated patients). Overall, nine patients reported serious adverse events, but none was thought to be related to the study drug. No clinical or subclinical cases of meningoencephalitis were recorded. In all, 67% CAD106-treated patients in cohort one and 82% in cohort two developed Aβ antibody response meeting the prespecified responder threshold. One of 12 placebo-treated patients (8%) had Aβ-IgG concentrations that qualified him as a responder. The study was published early online on June 6, 2012, in Lancet Neurology.

“Our findings suggest that CAD106 has a favorable safety profile and acceptable antibody response in patients with Alzheimer's disease,” concluded lead author Prof. Bengt Winblad, MD, PhD, of the Karolinska Institutet's AD Research Center. “Larger trials with additional dose investigations are needed to confirm the safety and establish the efficacy of CAD106.”

Aβ is the main component of amyloid plaques, found in the brains of patients with AD; the plaques are composed of a tangle of regularly ordered fibrillar aggregates called amyloid fibers. Recent research suggests that soluble oligomeric forms of the peptide may be causative agents in the development of AD, and a number of genetic, cell biology, biochemical and animal studies support the concept that Aβ plays a central role in the development of the pathology. The CAD106 treatment involves immunotherapy designed to induce N-terminal Aβ-specific antibodies without an Aβ-specific T-cell response.

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