Alzheimer’s disease (AD) has been reported for more than 100 years since its first discovery in 1906. There has been no significant progress in the study of its real causes and pathogenesis. The viewpoint of this paper is a heuristic viewpoint based on brain cell activation theory under such background. In this paper, the pathogenesis of sporadic AD is discussed at molecular level by applying the principles of cell physics and biology. The purpose of this paper is to harmonize the existing theories of etiology of AD and to solve the source problems that have plagued the research field of neurodegenerative diseases for a long time. Conclusion: (1) Basic contents: excess cations are transferred from extracellular to intracellular. They compete position with potassium ions on the inner surface of cell membranes, thus abatementing the membrane potential, making action potential unable to activate calcium channels normally, which eventually leads to abnormal apoptosis of brain cells. Amyloid plaque is the remains of abnormal apoptotic brain cells. Amyloid plaque is the aggregation of amyloid spots by van der Waals force and electrostatic attraction, and its interstitium is amyloid protein. Brain cells consist of neurons, microglia and astrocytes in turn. Most of the spotted nuclei in the remains are cations. (2) Solutions: physical means, especially transcranial magnetoelectricity stimulation, should be the first choice for treatment. (3) Naming principles: because of the core point of view in this paper—The position of cation occupying potassium is the initiating factor of AD, so the etiology theory is named theory of dove-like particles. Take the Chinese idiom “Turtledove occupies the nest of magpies”. “Turtledove” represents the non-essential cation, “magpie” refers to the effective potassium ion, and “nest” refers to the position of the effective potassium ion.