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Genetic co-regulation of neopterin and Parkinson’s disease
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Genetic co-regulation of neopterin and Parkinson’s disease
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Journal Article
Genetic co-regulation of neopterin and Parkinson’s disease
2026
Overview
Neopterin is a pro-inflammatory molecule upregulated in several diseases; however, its role in pathophysiology is unclear and its genetic regulation is unexplored. We observed that neopterin levels increase during senescence (
P-value
= 1.88×10
-13
,
beta
= 0.96) and positively correlate with age-related neurodegeneration and inflammation markers. The heritability estimation of neopterin variation was 35%. We then conducted a genome-wide association study on 999 Sardinians, identifying two signals in the GTP cyclohydrolase (GCH1) gene that were suggestively associated with neopterin levels. The first signal, led by rs140884539-C (
P-value
= 7.05×10
-08
,
beta
= 0.59), was in strong linkage disequilibrium with variants associated with predisposition to rheumatoid arthritis, decrease in dopamine, increased levels of
GCH1
transcript, dopamine metabolites, and galectin-3. The second signal, represented by rs12323905-T (
P-value
= 8.17×10
-08
,
beta
= 0.30), colocalised with
GCH1
splicing and Parkinson’s disease signals. Transcriptome analysis of 605 Sardinians showed that the Parkinson’s disease-predisposing variant was significantly associated with an increase in a shorter and inactive form of GCH1, whose presence is predicted to reduce the GCH1 decamer stability. The GCH1 homo-decamer regulates neopterin and tetrahydrobiopterin production, a cofactor required for the synthesis of dopamine and serotonin. Our data motivate experimental work to test whether modulating
GCH1
expression or isoform ratio alters dopaminergic function in Parkinson’s disease models.
