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In addition to its two major pathological hallmarks, extracellular amyloid beta (A\u03b2) plaques and intracellular neurofibrillary tangles (NFTs), recent evidence highlights the critical roles of mitochondrial dysfunction and neuroinflammation in disease progression. A\u03b2 impairs mitochondrial function, which, in part, can subsequently trigger inflammatory cascades, creating a vicious cycle of neuronal damage. Estrogen receptors (ERs) are widely expressed throughout the brain, and the sex hormone 17\u03b2-estradiol (E2) exerts neuroprotection through both anti-inflammatory and mitochondrial mechanisms. While E2 exhibits neuroprotective properties, its mechanisms against A\u03b2 toxicity remain incompletely understood. In this study, we investigated the neuroprotective effects of E2 against A\u03b2-induced mitochondrial dysfunction and neuroinflammation in primary cortical neurons, with a particular focus on the role of AMP-activated protein kinase (AMPK). We found that E2 treatment significantly increased phosphorylated AMPK and upregulated the expression of mitochondrial biogenesis regulator peroxisome proliferator-activated receptor gamma coactivator-1 \u03b1 (PGC-1\u03b1), leading to improved mitochondrial respiration. In contrast, A\u03b2 suppressed AMPK and PGC-1\u03b1 signaling, impaired mitochondrial function, activated the pro-inflammatory nuclear factor kappa-light-chain enhancer of activated B cells (NF-\u03baB), and reduced neuronal viability. E2 pretreatment also rescued A\u03b2-induced mitochondrial dysfunction, suppressed NF-\u03baB activation, and, importantly, prevented the decline in neuronal viability. However, the pharmacological inhibition of AMPK using Compound C (CC) abolished these protective effects, resulting in mitochondrial collapse, elevated inflammation, and cell death, highlighting AMPK\u2019s critical role in mediating E2\u2019s actions. Interestingly, while NF-\u03baB inhibition using BAY 11-7082 partially restored mitochondrial respiration, it failed to prevent A\u03b2-induced cytotoxicity, suggesting that E2\u2019s full neuroprotective effects rely on broader AMPK-dependent mechanisms beyond NF-\u03baB suppression alone. Together, these findings establish AMPK as a key mediator of E2\u2019s protective effects against A\u03b2-driven mitochondrial dysfunction and neuroinflammation, providing new insights into estrogen-based therapeutic strategies for AD.<\/jats:p>","DOI":"10.3390\/ijms26136203","type":"journal-article","created":{"date-parts":[[2025,7,1]],"date-time":"2025-07-01T05:28:28Z","timestamp":1751347708000},"page":"6203","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Estradiol Prevents Amyloid Beta-Induced Mitochondrial Dysfunction and Neurotoxicity in Alzheimer\u2019s Disease via AMPK-Dependent Suppression of NF-\u03baB Signaling"],"prefix":"10.3390","volume":"26","author":[{"given":"Pranav","family":"Mishra","sequence":"first","affiliation":[{"name":"Division of Neurodegenerative & Neurodevelopmental Disorders, St. Boniface Hospital Albrechtsen Research Centre, University of Manitoba, Winnipeg, MB R2H 2A6, Canada"},{"name":"Department of Pharmacology and Therapeutics, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R2H 2A6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ehsan K.","family":"Esfahani","sequence":"additional","affiliation":[{"name":"Division of Neurodegenerative & Neurodevelopmental Disorders, St. Boniface Hospital Albrechtsen Research Centre, University of Manitoba, Winnipeg, MB R2H 2A6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9507-1201","authenticated-orcid":false,"given":"Paul","family":"Fernyhough","sequence":"additional","affiliation":[{"name":"Division of Neurodegenerative & Neurodevelopmental Disorders, St. Boniface Hospital Albrechtsen Research Centre, University of Manitoba, Winnipeg, MB R2H 2A6, Canada"},{"name":"Department of Pharmacology and Therapeutics, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R2H 2A6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benedict C.","family":"Albensi","sequence":"additional","affiliation":[{"name":"Division of Neurodegenerative & Neurodevelopmental Disorders, St. Boniface Hospital Albrechtsen Research Centre, University of Manitoba, Winnipeg, MB R2H 2A6, Canada"},{"name":"Department of Pharmacology and Therapeutics, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R2H 2A6, Canada"},{"name":"Department of Pharmaceutical Sciences, Barry & Judy Silverman College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL 33328, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,6,27]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"445","DOI":"10.31887\/DCNS.2013.15.4\/hjahn","article-title":"Memory loss in Alzheimer\u2019s disease","volume":"15","author":"Jahn","year":"2013","journal-title":"Dialogues Clin. 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