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The present experiment tests whether overexpression of the gene for Bcl\u2010<jats:sub>X<\/jats:sub>L can inhibit excitotoxicity in this model system. To track Bcl\u2010<jats:sub>X<\/jats:sub>L expression, the gene for green fluorescent protein (GFP) was inserted in\u2010frame, upstream of the Bcl\u2010<jats:sub>X<\/jats:sub>L gene. The GFP\u2010Bcl\u2010<jats:sub>X<\/jats:sub>L gene was then cloned into an adeno\u2010associated viral (AAV2) vector. GFP expression in both SH\u2010SY5Y and embryonic day 15 (E15) motor neurons (MNs) peaked 48 hours after infection. Bcl\u2010<jats:sub>X<\/jats:sub>L expression in SH\u2010SY5Y cells significantly reduced terminal deoxy\u2010UTP nick\u2010end labeling (TUNEL)\u2013positive cells and maintained cell density after glutamate exposure. Similarly, Bcl\u2010<jats:sub>X<\/jats:sub>L expression inhibited the development of TUNEL staining in E15 MNs and supported cell density after glutamate exposure. These findings suggest that AAV\u2010mediated expression of genes for antiapoptotic proteins may provide a means for ALS gene therapy. Muscle Nerve, 2005<\/jats:p>","DOI":"10.1002\/mus.20418","type":"journal-article","created":{"date-parts":[[2005,8,22]],"date-time":"2005-08-22T22:20:48Z","timestamp":1124749248000},"page":"734-744","source":"Crossref","is-referenced-by-count":19,"title":["Neuroprotective adeno\u2010associated virus Bcl\u2010<sub>x<\/sub>L gene transfer in models of motor neuron disease"],"prefix":"10.1002","volume":"32","author":[{"given":"Mary E.","family":"Garrity\u2010Moses","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qingshan","family":"Teng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diana","family":"Tanase","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas 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