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Emerging evidence suggests an intricate genetic architecture in motor neuron diseases (MNDs), involving not only monogenic causes but also, to varying extents, risk alleles and oligogenic or polygenic contributions [1-3].The potential for shared genetic risk across related diseases has motivated us to examine the contributions of rare variants in canonical and non-canonical diseaseassociated genes in a group of MNDs to understand the † Gang Wu and Michael Benatar contributed equally.
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Wu et al. (2025) studied this question.
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