From OMIM
SCA17 is a neurologic disorder characterized by cerebellar ataxia, pyramidal and extrapyramidal signs, cognitive impairment, psychosis, and seizures. Most patients have onset of symptoms after age 30, although earlier onset has been reported. The clinical phenotype and inheritance pattern are similar to Huntington disease (HD; 143100) (Gao et al., 2008). SCA17 shows a complex pattern of inheritance, including autosomal dominant, autosomal dominant with incomplete penetrance, and digenic (see MOLECULAR GENETICS) depending on the size of the TBP repeat expansion. Unaffected individuals have between 25 and 41 CAG/CAA repeats in the TBP gene. Alleles with 47 or more CAG/CAA repeats are fully penetrant for SCA17. Alleles with 'intermediate expansions' between 41 and 46 repeats show incomplete penetrance. However, patients with intermediate TBP expanded alleles in combination with heterozygous mutations in the STUB1 gene (607207) demonstrate full penetrance of the disease, suggesting that intermediate SCA17 is actually a digenic disease and may represent the same entity as SCA48 (618093), which has a similar phenotype (Magri et al., 2022). Rarely, SCA17 has been found to be caused by homozygous or compound heterozygous TBP repeat expansions, consistent with autosomal recessive inheritance. For a general discussion of autosomal dominant of spinocerebellar ataxia, see SCA1 (164400).  http://www.omim.org/entry/607136

From MedlinePlus Genetics
As its name suggests, a Huntington's disease-like (HDL) syndrome is a condition that resembles Huntington's disease. Researchers have described four HDL syndromes, designated Huntington's disease-like 1 (HDL1) through Huntington's disease-like 4 (HDL4). These progressive brain disorders are characterized by uncontrolled movements, emotional problems, and loss of thinking ability. HDL syndromes occur in people with the characteristic features of Huntington's disease who do not have a variant (also called mutation) in the gene typically associated with that disorder.

HDL1, HDL2, and HDL4 usually appear in early to mid-adulthood, although they can begin earlier in life. The first signs and symptoms of these conditions often include irritability, emotional problems, small involuntary movements, poor coordination, and trouble learning new information or making decisions. Many affected people develop involuntary jerking or twitching movements known as chorea. As the disease progresses, these abnormal movements become more pronounced. Affected individuals may develop problems with walking, speaking, and swallowing. People with these disorders also experience changes in personality and a decline in thinking and reasoning abilities. Individuals with an HDL syndrome can live for a few years to more than a decade after signs and symptoms begin.

HDL3 begins much earlier in life than most of the other HDL syndromes (usually around age 3 or 4). Affected children experience a decline in thinking ability, difficulties with movement and speech, and seizures. Because HDL3 has a somewhat different pattern of signs and symptoms and a different pattern of inheritance, researchers are unsure whether it belongs in the same category as the other HDL syndromes.  https://medlineplus.gov/genetics/condition/huntingtons-disease-like-syndrome