History
Ataxia as a symptom was first described by French neurologist Duchenne de Boulogne in a subject with tabes dorsalis. By the late 19th and early 20th centuries, extensive research into the characterization, cause, and diagnostics of hereditary cerebellar ataxias was underway with the work of several prominent neurologists, including Jean-Martin Charcot, Pierre Marie, Nikolaus Friedreich, Adolph Strümpell, and others. Marie described a number of cases of hereditary, adult onset disease he thought to be clinically distinct from Friedreichs ataxia, spastic paraplegia, and other known types of ataxia, calling the syndrome hereditary cerebellar ataxia, though it became known Maries ataxia.While the hereditary patterns were clearly distinct, there was on-going debate well into the 1940s over whether Maries ataxia was really distinct from Freidreichs ataxia and Strümpells paraplegia and if these categorys themselves represented a single disease or many. This was because of the heterogenous nature of hereditary ataxias, the similarity of symptoms, and the lack of understood biochemical mechanisms. Further frustration with the ambiguity of terms introduced by Marie and Friedreich resulted in the creation of other systems to classify ataxias. Gordon Morgan Holmes and Godwin Greenfield each developed systems of categorizing ataxias, giving rise to categories called olivopontocerebellar atrophy and spinocerebellar degradation, though little consensus between the systems was achieved, and many terms are used interchangeably.In the depression era United States, the Schut family in Minnesota was one family known to carry a hereditary ataxia.
Positive results have been found in mice models using both stem cells from fetal neuroectoderm and adult stem cells from the lateral ventricles and the dentate gyrus. : 177–188  Using harvested stem cells in stem cell therapies require immunosuppression to prevent the host from rejecting the transplants; creating induced pluripotent stem cells from the hosts own cells would mitigate this risk and has had some testing in other neurodegenerative diseases. : 177–188 


== References ==