This article considers Alzheimer’s disease as a multifactorial condition that extends beyond the classical amyloid hypothesis and encompasses immune, inflammatory, and environmental mechanisms. It is shown that β-amyloid may function as an antimicrobial peptide of the innate immune system, allowing its accumulation to be interpreted as a response to chronic antigenic stimulation. Particular attention is given to neuroinflammation and microglial activation as key processes sustaining neurodegeneration. The role of infectious factors as potential triggers is discussed, and the concept of a quasi-infectious process is introduced to reflect the similarity between underlying immune mechanisms and classical infectious responses. The article also examines microplastics as a novel environmental cofactor capable of enhancing oxidative stress, inflammation, and barrier dysfunction. The synergistic interaction between aging, immune dysregulation, and environmental influences in shaping disease progression is emphasized. An integrative model of pathogenesis is proposed, unifying neuroimmune and environmental aspects of the disease.