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These degenerative and progressive diseases share some risk factors. To a large extent, the amyloid cascade is responsible for AD development. Neurofibrillary tangles induce neurodegeneration and brain atrophy; this chain reaction begins with hyperphosphorylation of tau proteins caused by progressive amyloid beta (A\u03b2) accumulation. In addition to these processes, it seems that alterations in brain glucose metabolism and insulin signalling lead to cell death and reduced synaptic plasticity in AD, before the onset of symptoms, which may be years away. Due to the substantial evidence linking insulin resistance in the brain with AD, researchers have coined the name \u201cType 3 diabetes\u201d to characterize the condition. We still know little about the processes involved, even though current animal models have helped illuminate the links between T2DM and AD. This brief overview discusses insulin and IGF\u20101 signalling disorders and the primary molecular pathways that may connect them. The presence of GSK\u20103\u03b2 in AD is intriguing. These proteins' association with T2DM and pancreatic \u03b2\u2010cell failure suggests they might be therapeutic targets for both disorders.<\/jats:p>","DOI":"10.1002\/cbf.4111","type":"journal-article","created":{"date-parts":[[2024,9,4]],"date-time":"2024-09-04T01:29:05Z","timestamp":1725413345000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Association Between Type 2 Diabetes Mellitus and Alzheimer's Disease: Common Molecular Mechanism and Therapeutic Targets"],"prefix":"10.1002","volume":"42","author":[{"given":"Aparna","family":"Chauhan","sequence":"first","affiliation":[{"name":"Department of Pharmacy School of Chemical Sciences and Pharmacy, Central University of Rajasthan  Rajasthan India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sachin","family":"Dubey","sequence":"additional","affiliation":[{"name":"Department of Pharmacy School of Chemical Sciences and Pharmacy, Central University of Rajasthan  Rajasthan India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3374-5792","authenticated-orcid":false,"given":"Smita","family":"Jain","sequence":"additional","affiliation":[{"name":"Department of Pharmacy School of Chemical Sciences and Pharmacy, Central University of Rajasthan  Rajasthan India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2024,9,3]]},"reference":[{"key":"e_1_2_18_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(84)90186-4"},{"key":"e_1_2_18_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneuro0124"},{"key":"e_1_2_18_4_1","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.53.2.474"},{"key":"e_1_2_18_5_1","doi-asserted-by":"publisher","DOI":"10.1007\/s007020050067"},{"key":"e_1_2_18_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jns.2005.08.017"},{"key":"e_1_2_18_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.exger.2006.08.009"},{"key":"e_1_2_18_8_1","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.53.9.1937"},{"key":"e_1_2_18_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF01219652"},{"key":"e_1_2_18_10_1","first-page":"151","article-title":"Islet Amyloid, Increased A\u2010Cells, Reduced B\u2010Cells and Exocrine Fibrosis: Quantitative Changes in the Pancreas in Type 2 Diabetes","volume":"9","author":"Clark A.","year":"1988","journal-title":"Diabetes Research"},{"key":"e_1_2_18_11_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.23.8628"},{"key":"e_1_2_18_12_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.11.3881"},{"issue":"1","key":"e_1_2_18_13_1","first-page":"1","article-title":"Immunolocalization of Islet Amyloid Polypeptide (IAPP) in Pancreatic Beta Cells by Means of Peroxidase\u2010Antiperoxidase (PAP) and Protein A\u2010Gold Techniques","volume":"130","author":"Johnson K. 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