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Unfortunately, there are no effective or long\u2010terms treatments capable of slowing down the relentless loss of neurons in any of these diseases. One impediment is the lack of detailed knowledge of the molecular mechanisms underlying the processes of neurodegeneration. While some neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, are mostly sporadic in nature, driven by both environment and genetic susceptibility, many others, including Huntington's disease, spinocerebellar ataxias, and spinal\u2010bulbar muscular atrophy, are genetically inherited disorders. Surprisingly, given their different roots and etiologies, both sporadic and genetic neurodegenerative disorders have been linked to disease mechanisms involving histone deacetylase (\n                      <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>\n                      ) proteins, which consists of 18 family members with diverse functions. While most studies have implicated certain\n                      <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>\n                      subtypes in promoting neurodegeneration, a substantial body of literature suggests that other\n                      <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>\n                      proteins can preserve neuronal viability. Of particular interest, however, is the recent realization that a single\n                      <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>\n                      subtype can have both neuroprotective and neurotoxic effects. Diverse mechanisms, beyond transcriptional regulation have been linked to these effects, including deacetylation of non\u2010histone proteins, protein\u2013protein interactions, post\u2010translational modifications of the\n                      <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>\n                      proteins themselves and direct interactions with disease proteins. The roles of these\n                      <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>\n                      s in both sporadic and genetic neurodegenerative diseases will be discussed in the current review.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc14309-fig-0002-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  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