
The study reveals that ATP10D—not GBA1—primarily regulates plasma GlcCer levels. Despite associations with Parkinson’s, GlcCer isn't a causal factor or disease predictor. Analysis of 489 individuals and 2.1 million variants confirms ATP10D’s stronger influence on GlcCer. With no genetic link between ATP10D and PD, the findings challenge GlcCer-based treatments and call for new therapeutic targets.
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