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Its main two hallmarks are extracellular deposition of aggregated amyloid beta resulting in senile plaques and intracellular hyperphosphorylated tau proteins forming neuro-fibrillary tangles. As those processes are promoted by the glycogen synthase kinase-3 enzyme, GSK3 inhibitors may be of therapeutic value in SAD. GSK3 is also inhibited by the action of insulin on insulin signaling. Insulin receptor desensitization in the brain is hypothesized to cause inhibition of insulin signaling pathway that ultimately causes cognitive deficits seen in SAD. In extant research, induction of cognitive impairment is achieved by intracerebroventricular injection of streptozotocin\u2014a diabetogenic compound that causes desensitization to insulin receptors in the brain leading to the appearance of most of the SAD signs and symptoms. Valproic acid \u2014a histone deacetylase inhibitor and anti-epileptic drug\u2014has been recently studied in the management of SAD as a possible GSK3 inhibitor. Accordingly, the aim of the present study is to explore the role of multiple VPA doses on the downstream effects of the insulin signaling pathway in ICV STZ-injected mice and suggest a possible mechanism of VPA action. ICV STZ-injected mice showed deficiency in short- and long-term memory as well as increased anxiety, as established by open field test, Modified Y-maze, Morris water maze, and elevated plus maze neurobehavioral tests.<\/jats:p>","DOI":"10.1007\/s10787-025-01695-0","type":"journal-article","created":{"date-parts":[[2025,3,19]],"date-time":"2025-03-19T20:43:04Z","timestamp":1742416984000},"page":"2083-2094","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Modulation of the cognitive impairment associated with Alzheimer\u2019s disease by valproic acid: possible drug repurposing"],"prefix":"10.1007","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7469-5886","authenticated-orcid":false,"given":"Mirna Ezzat Sedrak","family":"Sorial","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ragwa Mansour","family":"Abdelghany","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nesrine Salah El Dine","family":"El Sayed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,3,19]]},"reference":[{"issue":"4","key":"1695_CR1","doi-asserted-by":"publisher","first-page":"779","DOI":"10.1016\/j.neuropharm.2009.01.005","volume":"56","author":"R Agrawal","year":"2009","unstructured":"Agrawal R, Tyagi E, Shukla R, Nath C (2009) A study of brain insulin receptors, AChE activity and oxidative stress in rat model of ICV STZ induced dementia. 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