GM1 glangliosidosis is caused when the body does not produce enough of a specific enzyme called β-galactosidase (βgal), which recycles molecules from the body. When the molecules build to abnormal levels, they progressively destroy the body’s nervous system. The earlier the onset in children, the quicker the disease kills. Researchers have developed a treatment for GM1 gangliosidosis using AAV gene therapy by re-engineered the virus to introduce the gene that produces βgal. The virus acts as a vessel, its genetic material removed and replaced with a concentrated dose of the βgal gene. Healthy cells pass along βgal, essentially allowing deficient cells to soak in the crucial enzyme. The experimental therapy has extended the lives of cats, which have a similar genetic defect, from an average of eight months to more than 52 months, with no ill effects and with normal function.