Autosomal recessive spinocerebellar ataxia 12: genes and variants

Autosomal recessive spinocerebellar ataxia 12 is linked to 2 analyzed proteins (WWOX and SPTBN2). 7 DNA variants are known to cause it; 370 more are uncertain, and 0 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Also known as: autosomal recessive spinocerebellar ataxia 14

Genes linked to Autosomal recessive spinocerebellar ataxia 12

Known disease-causing variants in Autosomal recessive spinocerebellar ataxia 12

VariantPositionProtein partClinical label
WWOX G372R372Interaction with MAPTDisease-causing (★★)
WWOX Q230P230Mediates targeting to the mitochondriaDisease-causing (★★)
WWOX M1T1Disease-causing (★)
WWOX M1L1Disease-causing (★)
SPTBN2 R1482W1482Spectrin 11Disease-causing (★)
SPTBN2 R414C414Spectrin 1Disease-causing
WWOX P47T47WW 1Disease-causing

Same protein, different disease

Diseases related to Autosomal recessive spinocerebellar ataxia 12

Frequently asked questions

Which genes are linked to Autosomal recessive spinocerebellar ataxia 12?

In CATVariant, Autosomal recessive spinocerebellar ataxia 12 is linked to 2 analyzed proteins: WWOX (WW domain-containing oxidoreductase) and SPTBN2 (Spectrin beta chain, non-erythrocytic 2).

How many genetic variants are linked to Autosomal recessive spinocerebellar ataxia 12?

411 variants: 7 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 370 are of uncertain significance or have conflicting reports.

Which uncertain variants in Autosomal recessive spinocerebellar ataxia 12 look disease-causing?

None of the uncertain variants currently reaches the likely-pathogenic range on computable evidence alone.

About this data

Variant–disease links come from ClinVar, Open Targets and UniProt, pooled from the latest public CATVariant analysis of each human protein. Evidence scores use the ACMG/AMP Bayesian points scale with computable criteria only (position among known disease variants, rarity in gnomAD, calibrated predictors, deep mutational scanning); there is no family or patient data, so they prioritise variants for expert review and never classify them.

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