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A similar pathology is seen in specific myelin mutant mice that model \u2018advanced brain aging\u2019 and exhibit a range of behavioral abnormalities. However, the cognitive assessment of these mutants is problematic because myelin-dependent motor-sensory functions are required for quantitative behavioral readouts. To better understand the role of cortical myelin integrity for higher brain functions, we generated mice lacking\n                    <jats:italic>Plp1<\/jats:italic>\n                    , encoding the major integral myelin membrane protein, selectively in ventricular zone stem cells of the mouse forebrain. In contrast to conventional\n                    <jats:italic>Plp1<\/jats:italic>\n                    null mutants, subtle myelin defects were restricted to the cortex, hippocampus, and underlying callosal tracts. Moreover, forebrain-specific\n                    <jats:italic>Plp1<\/jats:italic>\n                    mutants exhibited no defects of basic motor-sensory performance at any age tested. Surprisingly, several behavioral alterations reported for conventional\n                    <jats:italic>Plp1<\/jats:italic>\n                    null mice (Gould et al., 2018) were absent and even social interactions appeared normal. However, with novel behavioral paradigms, we determined catatonia-like symptoms and isolated executive dysfunction in both genders. This suggests that loss of myelin integrity has an impact on cortical connectivity and underlies specific defects of executive function. These observations are likewise relevant for human neuropsychiatric conditions and other myelin-related diseases.\n                  <\/jats:p>","DOI":"10.7554\/elife.70792","type":"journal-article","created":{"date-parts":[[2023,1,30]],"date-time":"2023-01-30T12:15:54Z","timestamp":1675080954000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.70792","source":"Crossref","is-referenced-by-count":7,"title":["Isolated catatonia-like executive dysfunction in mice with forebrain-specific loss of myelin integrity"],"prefix":"10.7554","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7083-1358","authenticated-orcid":true,"given":"Sahab","family":"Arinrad","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03av75f26","id-type":"ROR","asserted-by":"publisher"}],"name":"Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences","place":["G\u00f6ttingen, 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