In our experimental model we found that 0.2 or 0.5 μM Aβ peptides characteristic for AD neuropathology (Aβ 1–42 and 1–40) as well as the derived neurotoxic decapeptide Aβ 25–35, are (even if not previously aggregated) by themselves able to trigger a presumably specific proliferative response of only a small proportion (around 1%) of CD4+CD28+ lymphocytes over up to 120 hours of contact in vitro. Here, CD4 is linked to Alzheimer disease.