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Acetyl\u2010CoA is potentially a key molecule in Schwann cells and oligodendrocytes because it is at the crossroads of cellular lipid biosynthesis and energy generation. The main route for acetyl\u2010CoA production is the oxidation of pyruvate by the pyruvate dehydrogenase complex (PDC). PDC deficiency in humans results in neurodegeneration and developmental impairments in both white and gray matter structures. To address the importance of PDC in myelinating glia, we deleted <jats:italic>Pdha1<\/jats:italic> gene specifically in oligodendrocytes and Schwann cells. Surprisingly, sciatic and optic nerve morphology and the motor performance of <jats:italic>Pdha1<\/jats:italic><jats:sup>f\/Y;<\/jats:sup> <jats:italic>Cnp<\/jats:italic><jats:sup>Cre\/+<\/jats:sup> mice are undistinguishable from those of controls at 1 month of age. In addition, myelin is stably maintained for at least 10 months. However, <jats:italic>Pdha1<\/jats:italic><jats:sup>f\/Y;<\/jats:sup> <jats:italic>Cnp<\/jats:italic><jats:sup>Cre\/+<\/jats:sup> mice showed reduced fiber density and signs of axonal degeneration in both sciatic and optic nerves from 6 months of age. In contrast, 10 month\u2010old mice bearing a floxed <jats:italic>Pdha1<\/jats:italic> gene with either P0\u2010Cre (expressed only by Schwann cells) or NG2\u2010Cre<jats:sup>ER<\/jats:sup> (expressed in oligodendrocyte precursor cells) do not show any sign of axonal pathology or alterations in myelin structure or thickness. This indicates that the axonopathy is specific to the <jats:italic>Pdha1<\/jats:italic><jats:sup>f\/Y;<\/jats:sup> <jats:italic>Cnp<\/jats:italic><jats:sup>Cre\/+<\/jats:sup> mice. Taken together, these results suggest that acetyl\u2010CoA derived from pyruvate is not necessary for myelin maintenance and, thus, myelin\u2010forming cells are not likely to contribute to the pathophysiology of PDC deficiency.<\/jats:p>","DOI":"10.1002\/glia.23184","type":"journal-article","created":{"date-parts":[[2017,6,28]],"date-time":"2017-06-28T10:15:57Z","timestamp":1498644957000},"page":"1626-1639","source":"Crossref","is-referenced-by-count":34,"title":["Acetyl\u2010CoA production from pyruvate is not necessary for preservation of myelin"],"prefix":"10.1002","volume":"65","author":[{"given":"Gustavo","family":"Della\u2010Flora Nunes","sequence":"first","affiliation":[{"name":"Hunter James Kelly Research Institute, University at Buffalo Buffalo New York 14203"},{"name":"Department of Biochemistry University at Buffalo Buffalo New York 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren","family":"Mueller","sequence":"additional","affiliation":[{"name":"Department of Biochemistry University at Buffalo Buffalo New York 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas","family":"Silvestri","sequence":"additional","affiliation":[{"name":"Deptartment of Neurology Jacobs School of Medicine and Biomedical Sciences, University at Buffalo Buffalo New York 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mulchand S.","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Biochemistry University at Buffalo Buffalo New York 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lawrence","family":"Wrabetz","sequence":"additional","affiliation":[{"name":"Hunter James Kelly Research Institute, University at Buffalo Buffalo New York 14203"},{"name":"Department of Biochemistry University at Buffalo Buffalo New York 14203"},{"name":"Deptartment of Neurology Jacobs School of Medicine and Biomedical Sciences, University at Buffalo Buffalo New York 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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