{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T23:20:20Z","timestamp":1792106420196,"version":"4.4.0"},"reference-count":267,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T00:00:00Z","timestamp":1765238400000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2025,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Main Problems<\/jats:title>\n                    <jats:p>The accumulation of amyloid beta (A\u03b2) plaques and neurofibrillary tangles (NFTs) composed of Tau protein is two characteristic brain pathologies in Alzheimer's disease (AD). However, the A\u03b2 hypothesis has recently faced challenges due to the limited clinical efficacy of anti\u2010A\u03b2 antibodies, such as aducanumab and lecanemab.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This comprehensive review highlights recent advances and debates regarding the pathophysiology of A\u03b2 peptides and plaques in AD, as well as their use as biomarkers and drug targets.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>A\u03b2 aggregation is primarily driven by an imbalance between its generation from amyloid precursor protein (APP) and its clearance from the brain, processes influenced by various risk factors. The toxicity of amyloid plaques is affected by the accumulation of different A\u03b2 species with varying lengths and post\u2010translational modifications of A\u03b2. Additionally, pathways including neuroinflammation, blood\u2013brain barrier deterioration, autophagy and mitochondrial dysfunction, lipid raft changes, and oxidative stress have pivotal roles in AD. Therefore, a clear map of A\u03b2's upstream regulators and downstream effectors is crucial for developing effective diagnostics and treatments for AD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Incorporating new research findings and ongoing debates surrounding the A\u03b2 cascade hypothesis is crucial for improving early diagnosis and for guiding the development of effective treatments for AD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.70688","type":"journal-article","created":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T10:57:20Z","timestamp":1765277840000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets"],"prefix":"10.1002","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0300-3226","authenticated-orcid":false,"given":"Shamseddin","family":"Ahmadi","sequence":"first","affiliation":[{"name":"Department of Biological Science, Faculty of Science University of Kurdistan  Sanandaj Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2311-9384","authenticated-orcid":false,"given":"Shiler","family":"Khaledi","sequence":"additional","affiliation":[{"name":"Department of Biological Science, Faculty of Science University of Kurdistan  Sanandaj Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-7046-7537","authenticated-orcid":false,"given":"Kimia","family":"Ahmadi","sequence":"additional","affiliation":[{"name":"Student Research Committee, School of Medicine Tabriz University of Medical Sciences  Tabriz Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8737-312X","authenticated-orcid":false,"given":"Kambiz","family":"Hassanzadeh","sequence":"additional","affiliation":[{"name":"Robert Wood Johnson Medical School, Institute for Neurological Therapeutics, and Department of Neurology Rutgers Biomedical and Health Sciences  Piscataway New Jersey 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