{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T04:33:06Z","timestamp":1790051586429,"version":"4.0.1"},"reference-count":327,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T00:00:00Z","timestamp":1778716800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:p>Despite many years of extensive research into the etiology and treatment of Alzheimer\u2019s disease, based on the importance of amyloid and tau protein as causative factors, these studies have stalled, have not brought any breakthroughs and, most importantly, have not led to any final conclusions. Therefore, the ineffectiveness of the above-mentioned actions and the pressure from the community of people affected by Alzheimer\u2019s disease forced the scientific community to change its way of thinking about the etiopathogenesis of this disease. This situation has prompted a group of scientists who have been studying the effects of brain ischemia for years to focus on post-ischemic changes, which\u2013similarly to Alzheimer\u2019s disease\u2013predominate in the hippocampus, leading to the development of amyloid plaques, neurofibrillary tangles and ultimately to dementia. In this context, it has been proposed that brain ischemia may play an important role in driving amyloid and tau protein pathology in the development of Alzheimer\u2019s disease. In this review, we present an update of extensive experimental and clinical studies conducted over several years on the role of brain ischemia in the neuropathogenesis of Alzheimer\u2019s disease. Current advances in understanding the ischemic etiology of Alzheimer\u2019s disease have revealed dysregulation of Alzheimer\u2019s disease-associated genes, including secretases, amyloid precursor protein, apoptosis, autophagy, mitophagy, tau protein, \u03b1-synuclein, apolipoproteins, LRP1, and RAGE. This article presents the relationship between genes which dysregulation is a result of brain ischemia and the cellular and tissue neuropathology characteristic of Alzheimer\u2019s disease and their proteins. These observations clearly indicate that, following brain ischemia, changes occur in the expression of Alzheimer\u2019s disease-associated genes and in the folding of disease-associated proteins such as amyloid, tau protein, and \u03b1-synuclein. This leads to massive neuronal death and disruption of the neuronal network, ultimately leading to the development of Alzheimer\u2019s disease-like dementia. Data indicate common genomic and proteomic factors in brain ischemia and Alzheimer\u2019s disease. It seems that the brain ischemia model may be useful in determining the role of folding proteins and their genes dysregulation in Alzheimer\u2019s disease. In the future, manipulation of genes and proteins associated with ischemia and ischemia-induced Alzheimer\u2019s disease will likely provide new hope for developing causal therapies that are urgently needed to prevent or treat Alzheimer\u2019s disease. The innovative\/novel approach to the etiology of Alzheimer\u2019s disease presented in this review will provide stakeholders with a glimpse into the future.<\/jats:p>","DOI":"10.3389\/fcell.2026.1804251","type":"journal-article","created":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T05:41:23Z","timestamp":1778737283000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Genomic and proteomic conversion of brain ischemia to Alzheimer\u2019s disease"],"prefix":"10.3389","volume":"14","author":[{"given":"Ryszard","family":"Pluta","sequence":"first","affiliation":[{"name":"Department of Pathophysiology, Medical University of Lublin","place":["Lublin, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marzena","family":"U\u0142amek-Kozio\u0142","sequence":"additional","affiliation":[{"name":"Department of Neurology, Institute of Psychiatry and Neurology","place":["Warsaw, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,5,14]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"172","DOI":"10.1016\/0304-3940(91)90020-t","article-title":"Selective induction of Kunitz-type protease inhibitor domain-containing amyloid precursor protein mRNA after persistent focal ischemia in rat cerebral cortex","volume":"125","author":"Abe","year":"1991","journal-title":"Neurosci. 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