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Their course is usually severe, leading to high morbidity and subsequent inability of patients to independent functioning. Vast majority of neurodegenerative diseases is currently untreatable, and only some symptomatic drugs are available which efficacy is usually very limited. To develop novel therapies for this group of diseases, it is crucial to understand their pathogenesis and to recognize factors which can influence the disease course. One of cellular structures which dysfunction appears to be relatively poorly understood in the light of neurodegenerative diseases is tubulin cytoskeleton. On the other hand, its changes, both structural and functional, can considerably influence cell physiology, leading to pathological processes occurring also in neurons. In this review, we summarize and discuss dysfunctions of tubulin cytoskeleton in various neurodegenerative diseases different than primary tubulinopathies (caused by mutations in genes encoding the components of the tubulin cytoskeleton), especially Alzheimer\u2019s disease, Parkinson\u2019s disease, Huntington\u2019s disease, amyotrophic lateral sclerosis, prion diseases, and neuronopathic mucopolysaccharidoses. It is also proposed that correction of these disorders might attenuate the progress of specific diseases, thus, finding newly recognized molecular targets for potential drugs might become possible.<\/jats:p>","DOI":"10.1007\/s10571-022-01304-6","type":"journal-article","created":{"date-parts":[[2022,11,9]],"date-time":"2022-11-09T21:20:20Z","timestamp":1668028820000},"page":"1867-1884","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Tubulin Cytoskeleton in Neurodegenerative Diseases\u2013not Only Primary Tubulinopathies"],"prefix":"10.1007","volume":"43","author":[{"given":"Zuzanna","family":"Cyske","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lidia","family":"Gaffke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karolina","family":"Pierzynowska","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4042-7466","authenticated-orcid":false,"given":"Grzegorz","family":"W\u0119grzyn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,11,9]]},"reference":[{"key":"1304_CR1","doi-asserted-by":"crossref","DOI":"10.15252\/embj.2018101023","volume":"37","author":"A Akhmanova","year":"2018","unstructured":"Akhmanova A, Hoogenraad CC (2018) More is not always better: hyperglutamylation leads to neurodegeneration. 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