I believe HD to be an autoimmune disorder for the reasons discussed in CAG v. Immune System. HD remains obscure for most researchers. I was encouraged by Dr. Horrobin's suggestion that HD may be 'arthritis of the brain'. Now another researcher suggests that some ataxias (caused by a CAG expansion) may be immune related.

The resolution of HD as an autoimmune disorder is important. There are many immune related therapies that may work for HD. --Jerry 02Feb01
Curr Opin Neurol 2000 Aug;13(4):451-5, Klockgether T.

Since the discovery of the first mutations that cause hereditary ataxias in the early 1990s, there has been continuous progress in deciphering the molecular pathogenesis of degenerative ataxias.

Recent research in Friedreich's ataxia, the most frequent recessive ataxia, has provided further evidence that the clinical phenotype of this disorder is caused by abnormal oxidative phosphorylation due to mitochondrial dysfunction.

The dominantly inherited spinocerebellar ataxias (SCAs) are genetically heterogeneous. Up to now, 11 distinct loci have been identified. The mutations that cause SCA1, SCA2, SCA3, SCA6 and SCA7 share the common feature of an expanded CAG sequence, encoding an abnormally long polyglutamine tract within the respective gene products.

Recent pathogenetic research points to the importance of abnormal protein-protein interaction and altered gene transcription. The aetiology of many sporadic ataxias remains obscure. In some patients, association of ataxia with specific serum antibodies (antigliadin, antiglutamic acid decarboxylase) suggests an immune pathogenesis.