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Here, we show that ASC transplantation rescues the striatal pathology of Huntington disease (HD) models.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>ASCs were isolated from human subcutaneous adipose tissue. In a quinolinic acid (QA)\u2010induced rat model of striatal degeneration, human ASCs (1 million cells) were transplanted into the ipsilateral striatal border immediately after the QA injection. In 60\u2010day\u2010old R6\/2 mice transgenic for HD, ASCs (0.5 million cells) were transplanted into each bilateral striata. In in vitro experiments, we treated mutant huntingtin gene\u2010transfected cerebral neurons with ASC\u2010conditioned media.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In the QA model, human ASCs reduced apomorphine\u2010induced rotation behavior, lesion volume, and striatal apoptosis. In R6\/2 transgenic mice, transplantation of ASCs improved Rota\u2010Rod performance and limb clasping, increased survival, attenuated the loss of striatal neurons, and reduced the huntingtin aggregates. ASC\u2010transplanted R6\/2 mice expressed elevated levels of peroxisome proliferator\u2010activated receptor \u03b3 coactivator\u20101\u03b1 (PGC\u20101\u03b1) and reactive oxygen defense enzymes and showed activation of the Akt\/cAMP\u2010response element\u2010binding proteins. ASC\u2010conditioned media decreased the level of N\u2010terminal fragments of mutant huntingtin and associated apoptosis, and increased PGC\u20101\u03b1 expression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>Collectively, ASC transplantation slowed striatal degeneration and behavioral deterioration of HD models, possibly via secreted factors. 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