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• W2950803313 abstract "Objective: 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. Method: 1.Discuss the relationship with the existing hypothesis: the Aβ protein hypothesis, the tau protein hypothesis, the presenilin (PS) hypothesis, the apolipoprotein E (ApoE) hypothesis, the cholinergic hypothesis, the inflammatory hypothesis；2. Demonstration: biophysical proof, medical pathological proof, biological model proof; 3. Interpretation: ion channel and blood-brain barrier, potassium ion and potassium channel, ion pump and epilepsy and cancer, A beta protein and spots and plaques, related AD solutions. Result: 1. Abeta is not the cause of AD, but the late event of AD. 2. The K + concentration difference of 0.00001% which causes the great change of membrane potential is the effective concentration, which can not be neglected. 3. Abnormal impairment of potassium channels and early entry of sodium ions to occupy potassium positions are related to epilepsy, cancer and HeLa cells. 4. AD is a physical disease. especially transcranial magnetoelectricity stimulation, should be the first choice for treatment，which can activate abnormal neurons accurately without interfering with normal neurons. 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 are 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: the core viewpoint of this paper can be regarded as exploring the etiology of sporadic AD, it is companion volume of Brain cell activation theory, Brain cell activation theory is an explanation of the treatment methods and mechanism of neurodegenerative diseases such as AD, it is suitable for encephalopathy but not limited to encephalopathy, the solution of AD should start with prevention and treatment, the external factor of prevention is environment, especially heavy metal ions, the internal cause is body acidity and alkalinity, 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." @default.
• W2950803313 created "2019-06-27" @default.
• W2950803313 creator A5047201549 @default.
• W2950803313 date "2019-02-28" @default.
• W2950803313 modified "2023-09-23" @default.
• W2950803313 title "The theory of dove-like particles" @default.
• W2950803313 doi "https://doi.org/10.31219/osf.io/wsvcb" @default.
• W2950803313 hasPublicationYear "2019" @default.
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