{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T14:54:35Z","timestamp":1788188075806,"version":"build-2803163510"},"reference-count":123,"publisher":"MDPI AG","issue":"22","license":[{"start":{"date-parts":[[2024,11,20]],"date-time":"2024-11-20T00:00:00Z","timestamp":1732060800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Ministry of Education and Science for the Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland","award":["9\/2024"],"award-info":[{"award-number":["9\/2024"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>The abnormal deposition and intercellular propagation of disease-specific protein play a central role in the pathogenesis of many neurodegenerative disorders. Recent studies share the common observation that the formation of protein oligomers and subsequent pathological filaments is an essential step for the disease. Synucleinopathies such as Parkinson\u2019s disease (PD), dementia with Lewy bodies (DLB) or multiple system atrophy (MSA) are neurodegenerative diseases characterized by the aggregation of the \u03b1-synucleinprotein in neurons and\/or in oligodendrocytes (glial cytoplasmic inclusions), neuronal loss, and astrogliosis. A similar mechanism of protein Tau-dependent neurodegeneration is a major feature of tauopathies, represented by Alzheimer\u2019s disease (AD), corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), and Pick\u2019s disease (PD). The specific inhibition of the protein misfolding and their interneuronal spreading represents a promising therapeutic strategy against both disease pathology and progression. The most recent research focuses on finding potential applications targeting the pathological forms of proteins responsible for neurodegeneration. This review highlights the mechanisms relevant to protein-dependent neurodegeneration based on the most common disorders and describes current therapeutic approaches targeting protein misfolding and aggregation.<\/jats:p>","DOI":"10.3390\/ijms252212448","type":"journal-article","created":{"date-parts":[[2024,11,20]],"date-time":"2024-11-20T03:57:04Z","timestamp":1732075024000},"page":"12448","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Targeting Protein Misfolding and Aggregation as a Therapeutic Perspective in Neurodegenerative Disorders"],"prefix":"10.3390","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3916-7660","authenticated-orcid":false,"given":"Marta","family":"Sidoryk-W\u0119grzynowicz","sequence":"first","affiliation":[{"name":"Laboratory of Pathoneurochemistry, Department of Neurochemistry, Mossakowski Medical Research Institute, 02-106 Warsaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kamil","family":"Adamiak","sequence":"additional","affiliation":[{"name":"Laboratory of Pathoneurochemistry, Department of Neurochemistry, Mossakowski Medical Research Institute, 02-106 Warsaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lidia","family":"Stru\u017cy\u0144ska","sequence":"additional","affiliation":[{"name":"Laboratory of Pathoneurochemistry, Department of Neurochemistry, Mossakowski Medical Research Institute, 02-106 Warsaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,11,20]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1300","DOI":"10.1038\/s41593-018-0237-7","article-title":"Converging Pathways in Neurodegeneration, from Genetics to Mechanisms","volume":"21","author":"Gan","year":"2018","journal-title":"Nat. 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