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They display overlapping features consisting of both chronic and episodic neurological symptoms and usually show only a mild cerebellar atrophy in imaging studies, with prevalent involvement of the vermis. To evaluate cerebellar volumetry as a biomarker for distinguishing between these disorders and for understanding their neuroanatomical correlates. We applied a deep learning method (CerebNet) for the lobular segmentation and volumetry assessment of the cerebellum on 3.0 Tesla MRI scans of patients with genetically confirmed\n                    <jats:italic>CACNA1A<\/jats:italic>\n                    - (n\u2009=\u200916) and GAA-\n                    <jats:italic>FGF14<\/jats:italic>\n                    -related (n\u2009=\u200912) ataxia. K-means clustering and principal component analysis were employed to assess infratentorial atrophy patterns. Three distinct clusters based on the patterns of infratentorial volume loss were established, with vermian atrophy contributing the most. The degree of vermian atrophy was not correlated with the clinical severity of chronic ataxia, but with age at disease onset (\n                    <jats:italic>r<\/jats:italic>\n                    <jats:sub>\n                      <jats:italic>s<\/jats:italic>\n                    <\/jats:sub>\n                    (26)\u2009=\u20090.47,\u00a0\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.01). The cluster with most marked atrophy of the vermis comprised patients with missense\n                    <jats:italic>CACNA1A<\/jats:italic>\n                    variants who exhibited an early disease onset and migraine with aura as episodic manifestation. Conversely, there was an increase in the frequency of episodic ataxia and both loss-of-function\n                    <jats:italic>CACNA1A<\/jats:italic>\n                    variants and GAA-\n                    <jats:italic>FGF14<\/jats:italic>\n                    -expansions as genotypes when progressing from clusters with more to less severe vermian atrophy. Age at onset and the modality of channel dysfunction are key determinants of cerebellar volume loss in\n                    <jats:italic>CACNA1A<\/jats:italic>\n                    and\n                    <jats:italic>GAA-FGF14<\/jats:italic>\n                    -disease.\n                  <\/jats:p>","DOI":"10.1007\/s12311-026-01966-8","type":"journal-article","created":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T02:45:59Z","timestamp":1772592359000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genotype and Age at Onset Drive Vermis Atrophy in CACNA1A- and GAA-FGF14-related Ataxias"],"prefix":"10.1007","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0217-8630","authenticated-orcid":false,"given":"Elisabetta","family":"Indelicato","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang","family":"Nachbauer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Amprosi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Pellerin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephanie","family":"Mangesius","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elke R.","family":"Gizewski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9836-2514","authenticated-orcid":false,"given":"Stefan","family":"Kiechl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernhard","family":"Brais","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvia","family":"Boesch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Krismer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"name":"for the Alzheimer\u2019s Disease Neuroimaging Initiative","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,3,4]]},"reference":[{"issue":"6","key":"1966_CR1","doi-asserted-by":"publisher","first-page":"1579","DOI":"10.1093\/brain\/awx081","volume":"140","author":"M Coutelier","year":"2017","unstructured":"Coutelier M, Coarelli G, Monin ML, Konop J, Davoine CS, Tesson C, et al. 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