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Brain insulin resistance is influenced by inflammation, glycemia, and stress, and glucose uptake into the central nervous system is mediated by brain glucose transporter. Glucose hypometabolism leads to oxidative stress. During protein synthesis, DNA is vulnerable to being insulted by reactive oxygen species. If repair fails, the neuron undergoes apoptosis. If the repair is imperfect, it may synthesize an abnormal protein, which could induce an immune response. The resulting inflammation may initiate brain insulin resistance, leading to glucose hypometabolism. Integrating all these major factors forms an AD model. One factor impacts more other factors. This process becomes a vicious cycle, creating a positive feedback loop.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>AD-model application:<\/jats:title>\n                    <jats:p>The AD model should be able to explain the observable AD incidents. The amyloid-\u03b2 (A\u03b2) is extracellular, which would induce an immune response. On the contrary, tau and \u03b1-synuclein are intracellular proteins, which only cause an immune response if they leak out of the neuron. This is the reason why 2\/3 of dementia cases are AD. Besides living longer, women have more immune sensitivity compared to men, and postmenopausal women have higher insulin resistance and endothelial dysfunction due to a decline in estrogen production. This is the reason why women have twice the AD in comparison to men. Removing abnormal proteins or applying an anti-inflammatory agent could reduce inflammation; therefore, one-third of people remain cognitively normal despite the presence of A\u03b2 buildup in the brain.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/25424823251395616","type":"journal-article","created":{"date-parts":[[2025,11,10]],"date-time":"2025-11-10T17:07:15Z","timestamp":1762794435000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["Alzheimer's disease model explains Alzheimer\u2019s disease incidences"],"prefix":"10.1177","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0229-5186","authenticated-orcid":false,"given":"John Cheung-Yuen","family":"Chan","sequence":"first","affiliation":[{"name":"Independent Researcher"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,11,10]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.31887\/DCNS.2003.5.1\/hhippius"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.4103\/0019-5545.44908"},{"key":"e_1_3_3_4_2","unstructured":"Alzheimer\u2019s Disease International https:\/\/www.alzint.org\/about\/dementia-facts-figures\/ (accessed 24 July 2025)."},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms232213954"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1566067"},{"key":"e_1_3_3_7_2","first-page":"274128","article-title":"Amyloid-beta peptide, oxidative stress and inflammation in Alzheimer's disease: potential neuroprotective effects of omega-3 polyunsaturated fatty acids","volume":"2010","author":"Dyall SC","year":"2010","unstructured":"Dyall SC. 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