In young mice, Lactobacillus johnsonii NCC 533 (La1) treatment, was followed by significantly reduced CD80, CD86, and CTLA4 gene expression, which markedly inhibited the development of AD-like lesions, reduced the skin score, and impeded the overexpression of proinflammatory factors (including IL-8, IL-12, and IL-23). The gene discussed is CTLA4; the disease is Alzheimer disease.