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Accès ouvert déclaré 2026 article

Inflammation and neuropsychiatric symptoms in Parkinson's disease: a genetic association

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Background There has been some evidence that neuroinflammation is involved in Parkinson's disease (PD) and in psychiatric disorders. Objective To explore the effects of IL-1β rs16944 on PD patients' neuropsychiatric symptoms. Methods Two hundred and eighty-one consecutive PD patients underwent a neurological and neuropsychological evaluations, which included: Unified Parkinson's Disease Rating Scale, Schwab and England Activities of Daily Living scale, Questionnaire for Impulsive-Compulsive Disorders in Parkinson's Disease—Anytime Short, Hospital Anxiety and Depression Scale and Dementia Rating Scale-2. The Neuropsychiatric Inventory (NPI) was also applied to patients' caregivers/informants. In addition to IL-1β rs16944, DRD3 rs6280 and GRIN2B rs7301328 were also genotyped. Non-parametric group comparisons and linear and logistic regressions were used for data analyses. Results The IL-1β rs16944 (specifically TT vs. CC) genotype was associated with increased frequency of impulse-control behaviors and disorders (ICBDs) and impulse control disorders (ICDs; OR = 3.54, p = 0.004 and OR = 3.63, p = 0.006, respectively) and with more NPI reports of hallucinations (OR = 3.92, p = 0.014) and more neuropsychiatric symptoms (ß = 0.73, p = 0.019). The rs16944 T allele was related to more NPI reports of hallucinations (OR = 2.31, p = 0.032) and agitation/aggression (OR = 2.02, p = 0.039). Conclusion Study findings suggest that a polymorphism previously associated with increased IL-1β expression may increase the risk of certain neuropsychiatric symptoms in PD.

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DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.

Titre Crossref
Inflammation and neuropsychiatric symptoms in Parkinson's disease: a genetic association
Date Crossref
31/08/2026
Éditeur
Frontiers Media SA
Type
journal-article

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Institutions déclarées

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Sujets associés

Parkinson's Disease Mechanisms and TreatmentsTryptophan and brain disordersNeuroinflammation and Neurodegeneration Mechanisms

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