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Cholesterol metabolism has emerged as a critical factor involved with both central and peripheral dysregulation contributing to pathology. This review synthesizes current evidence on cholesterol's role in neurodegeneration and evaluates the therapeutic potential of statins, which act via cholesterol\u2010dependent and other pleiotropic mechanisms. A PubMed search covering 1985\u20132025 publications was conducted using terms related to neurodegenerative diseases, statins, cholesterol metabolism, neuroinflammation, oxidative stress, mitochondrial dysfunction, and neuroprotection. Studies were selected to highlight mechanistic insights into cholesterol regulation in the nervous system and clinical data on statin use. Neuronal loss in neurodegeneration is driven by processes including excitotoxicity, inflammation, and mitochondrial dysfunction. Excessive reactive oxygen species activate apoptotic pathways involving\n                    <jats:italic>BAX<\/jats:italic>\n                    ,\n                    <jats:italic>BAK<\/jats:italic>\n                    , and\n                    <jats:italic>p53<\/jats:italic>\n                    . Dysregulated cholesterol metabolism is a significant contributor: In AD, the\n                    <jats:italic>ApoE<\/jats:italic>\n                    allele\n                    <jats:italic>\u03b54<\/jats:italic>\n                    (\n                    <jats:italic>ApoE4<\/jats:italic>\n                    ) links elevated cholesterol to amyloid\u2010\u03b2 (A\u03b2) accumulation and cognitive decline; in PD, cholesterol shows mixed effects, with some studies suggesting protection and others linking high levels to \u03b1\u2010synuclein aggregation and mitochondrial impairment. In HD reduced cholesterol biosynthesis correlates with neuronal loss, while MS associates with elevated cholesterol and cognitive dysfunction. Statins, widely used cholesterol\u2010lowering agents, reduce A\u03b2 production, enhance its clearance, and improve synaptic function. Beyond lipid lowering, they exert anti\u2010inflammatory, antioxidant, and anti\u2010apoptotic effects. Clinical outcomes remain mixed, with benefits influenced by statin type, dose, treatment duration, disease stage, and patient genetics. Statins show multifaceted neuroprotective potential through cholesterol\u2010dependent and independent pathways. While preclinical data are encouraging, clinical evidence is heterogeneous. Long\u2010term, stratified trials are needed to clarify efficacy, and tailoring therapy to disease\u2010specific mechanisms may offer a viable strategy for mitigating neurodegeneration and enhancing neuronal survival.\n                  <\/jats:p>","DOI":"10.1002\/nep3.70026","type":"journal-article","created":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T05:25:06Z","timestamp":1771392306000},"page":"30-47","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Navigating the cholesterol maze: Key insights on use of statins in neurodegenerative disorders"],"prefix":"10.1002","volume":"4","author":[{"given":"Jun Han","family":"Kuan","sequence":"first","affiliation":[{"name":"Department of Pathology and Pharmacology, School of Medicine IMU University Kuala Lumpur Malaysia"},{"name":"Ninewells Hospital and Medical School School of Medicine, University of Dundee Dundee Scotland UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roshan S.","family":"Raghavan","sequence":"additional","affiliation":[{"name":"Department of Pathology and Pharmacology, School of Medicine IMU University Kuala Lumpur Malaysia"},{"name":"School of Undergraduate Medicine University of Glasgow Glasgow Scotland UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dawn Li Wei","family":"Koh","sequence":"additional","affiliation":[{"name":"Department of Pathology and Pharmacology, School of Medicine IMU University Kuala Lumpur Malaysia"},{"name":"School of Undergraduate Medicine University of Glasgow Glasgow Scotland UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-8909-4814","authenticated-orcid":false,"given":"Wing Yeng","family":"Tan","sequence":"additional","affiliation":[{"name":"Department of Pathology and Pharmacology, School of Medicine IMU University Kuala Lumpur Malaysia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2852-8486","authenticated-orcid":false,"given":"Igor","family":"Iezhitsa","sequence":"additional","affiliation":[{"name":"Department of Pathology and Pharmacology, School of Medicine IMU University Kuala Lumpur Malaysia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3050-7449","authenticated-orcid":false,"given":"Renu","family":"Agarwal","sequence":"additional","affiliation":[{"name":"Department of Pathology and Pharmacology, School of Medicine IMU University Kuala Lumpur Malaysia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,2,17]]},"reference":[{"key":"e_1_2_10_2_1","unstructured":"World Health Organization. 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