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Recent candidate gene studies in anorexia nervosa (AN) have included GPR55 (HGNC:4511) among a panel of genes assessed in a cohort of 135 Italian patients diagnosed by DSM‑V criteria (PMID:38112957). Although no individual GPR55 variant was described in detail, its recurrent inclusion in both case report and multi‑patient studies suggests a potential, albeit not fully characterized, role in the complex etiology of AN. The genetic data currently offer limited evidence; neither extensive segregation analyses nor robust variant‐level characterization has been performed to definitively link GPR55 alterations with AN pathology.
Functional assessments of GPR55, performed in separate studies, demonstrate the receptor’s involvement in CNS functions such as motor coordination and modulation of neurotransmission (PMID:23565223, PMID:28005346, PMID:37886574). However, these experimental observations, while highlighting biological relevance, do not directly confirm a mechanistic role in anorexia nervosa. Collectively, the genetic and experimental evidence currently provides a limited level of support for a direct gene‑disease association between GPR55 and AN.
Key take‑home: Although GPR55 is a promising candidate from multi‑gene panels, further detailed segregation and functional studies focused on AN are essential to establish its diagnostic and clinical utility.
Gene–Disease AssociationLimitedCandidate gene evidence from a study of 135 AN patients (PMID:38112957) that lacked detailed segregation and variant‐level data. Genetic EvidenceLimitedGPR55 was identified as a candidate in a multi‑gene panel study, but specific causal variants and further segregation evidence are not available (PMID:38112957). Functional EvidenceLimitedFunctional studies demonstrate GPR55’s role in CNS functions and neurotransmission (PMID:23565223, PMID:28005346, PMID:37886574), yet they do not directly link its function to anorexia nervosa pathogenesis. |