{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T13:31:06Z","timestamp":1789047066869,"version":"build-2803163510"},"reference-count":171,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T00:00:00Z","timestamp":1787616000000},"content-version":"vor","delay-in-days":24,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Brain and Behavior"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>Although Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and Huntington's disease (HD) present with markedly different clinical phenotypes, these neurodegenerative diseases (NDDs) appear to converge on a shared set of underlying molecular disturbances. This review sought to integrate disease\u2010specific causative triggers with shared pathogenic pathways, focusing on neuroinflammatory signaling, oxidative imbalance, mitochondrial impairment, and disrupted protein homeostasis, in order to support multi\u2010target, disease\u2010modifying therapeutic strategies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>Relevant classical and contemporary literature, encompassing original research and review articles on the molecular basis of AD, PD, ALS, MS, and HD, was reviewed and synthesized narratively, with attention to how neuroinflammatory and oxidative stress pathways intersect, reinforce one another through mitochondrial and inflammasome\u2010driven feedback, and recur across the five conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Finding<\/jats:title>\n                    <jats:p>In each disorder, persistently activated microglia and astrocytes secreted inflammatory mediators and reactive oxygen species, engaged the NLRP3 inflammasome, and progressively destabilized cellular homeostasis through a self\u2010perpetuating cycle linking neuroinflammation and oxidative stress. Disease\u2010specific lesions nonetheless persisted: amyloid\u2010\u03b2 and tau pathology in AD; \u03b1\u2010synuclein aggregation with iron\u2010driven mitochondrial damage in PD; RNA\u2010binding protein dysfunction, proteostatic collapse, and excitotoxicity in ALS; inflammatory demyelination and axonal bioenergetic failure in MS; and mutant huntingtin\u2010driven transcriptional and mitochondrial disruption in HD. These distinct triggers ultimately converged on shared downstream cascades.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Recognizing this shared pathogenic foundation supports multi\u2010target therapies\u2014such as Nrf2 activation, NLRP3 inhibition, mitochondria\u2010targeted antioxidants, and gene\u2010based interventions\u2014that extend across diagnostic boundaries, though challenges in intervention timing, patient stratification, and clinical translation remain unresolved.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/brb3.71615","type":"journal-article","created":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T04:21:55Z","timestamp":1787718115000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Unraveling Neurodegeneration: Common Molecular Mechanisms and Novel Therapeutic Concepts in Major Neurodegenerative Disorders"],"prefix":"10.1002","volume":"16","author":[{"given":"Fatemeh sadat","family":"Aldaghi","sequence":"first","affiliation":[{"name":"Department of Biology, Faculty of Science University of Guilan  Rasht Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zakieh","family":"Siahpoosh","sequence":"additional","affiliation":[{"name":"Department of Biology, Faculty of Science University of Guilan  Rasht Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6101-7189","authenticated-orcid":false,"given":"Zivar","family":"Salehi","sequence":"additional","affiliation":[{"name":"Department of Biology, Faculty of Science University of Guilan  Rasht Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Farhad","family":"Mashayekhi","sequence":"additional","affiliation":[{"name":"Department of Biology, Faculty of Science University of Guilan  Rasht Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shabnam","family":"Sohrabnezhad","sequence":"additional","affiliation":[{"name":"Faculty of Chemistry University of Guilan  Rasht 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