Alzheimer’s disease (AD) is the most well-known and most common type of age-related dementia. Amyloid deposition and hyperphosphorylation of tau protein are both pathological hallmarks of the AD. Using a triple-transgenic mouse model (3xTg-AD) that develops plaques and tangles in the brain similar to the human AD, we provide evidence that active full-length DNA amyloid-β peptide 1–42 (Aβ42) trimer immunization leads to the reduction of both amyloid and tau aggregation and accumulation.