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This work was supported by the University of Witten-Herdecke Germany.","award":["D753"],"award-info":[{"award-number":["D753"]}]},{"name":"Private Universit\u00e4t Witten\/Herdecke gGmbH"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Neuromol Med"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Alzheimer\u2019s disease (AD)is an age-related neurodegenerative disease  characterized by memory decline and cognitive impairment .AD is common in people aged &gt; 65 years, though  most of AD cases are sporadic, which accounts for 95%, and 1\u20135% of AD is caused by familial causes . The causes of AD are aging, environmental toxins, and cardiometabolic factors that induce the degeneration of cholinergic neurons. It has been shown that the metabolic syndrome which  is a clustering of dissimilar constituents including  insulin resistance (IR), glucose intolerance, visceral obesity, hypertension, and dyslipidemia is implicated in the pathogenesis of AD. Metabolic syndrome disapprovingly affects cognitive function and the development in AD by inducing the development of oxidative stress, neuroinflammation, and brain IR. These changes, together with brain IR, impair cerebrovascular reactivity causing cognitive impairment and dementia. Nevertheless, the fundamental mechanism by which metabolic syndrome persuades AD risk is not entirely explicated. Accordingly, this review aims to discuss the connotation between metabolic syndrome and AD. In conclusion, metabolic syndrome is regarded as a possible risk factor for the initiation of AD neuropathology by diverse signaling pathways such as brain IR, activation of inflammatory signaling pathways, neuroinflammation, defective proteostasis, and dysregulation of lipid mediators.<\/jats:p>","DOI":"10.1007\/s12017-025-08832-6","type":"journal-article","created":{"date-parts":[[2025,5,16]],"date-time":"2025-05-16T15:48:05Z","timestamp":1747410485000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["The Conceivable Role of Metabolic Syndrome in the Pathogenesis of Alzheimer\u2019s Disease: Cellular and Subcellular Alterations in Underpinning a Tale of Two"],"prefix":"10.1007","volume":"27","author":[{"given":"Ekremah A.","family":"Alzarea","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3097-2962","authenticated-orcid":false,"given":"Hayder M.","family":"Al-Kuraishy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8284-8897","authenticated-orcid":false,"given":"Ali I.","family":"Al-Gareeb","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2206-7236","authenticated-orcid":false,"given":"Athanasios","family":"Alexiou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9020-874X","authenticated-orcid":false,"given":"Marios","family":"Papadakis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4469-9266","authenticated-orcid":false,"given":"Olivia N.","family":"Beshay","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7817-425X","authenticated-orcid":false,"given":"Gaber El-Saber","family":"Batiha","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,5,16]]},"reference":[{"key":"8832_CR1","doi-asserted-by":"publisher","first-page":"159","DOI":"10.1016\/j.lfs.2017.11.005","volume":"193","author":"NF Abo El-Magd","year":"2018","unstructured":"Abo El-Magd, N. 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