Answers are grounded in this paper and cite their sources.
The occurrence and the tremendous phenotypic variability of late-onset neurolipidosis variants are explained on the basis of a simple kinetic model that describes the correlation between residual activity of a deficient lysosomal enzyme and the degradation rate of its substrate in the lysosome.
No takes yet. Share an insight, caveat, or question.
Conzelmann et al. (1991) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: