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The Possible Link Between Serum Lipocalin-2 Level and Mild Cognitive Impairment in Adults With Metabolic Syndrome

Introduction: Metabolic syndrome (MetS) is associated with an increased risk of cognitive impairment. Lipocalin-2 (LCN2) or neutrophil gelatinase-associated lipocalin (NGAL), is an inflammatory protein, and participates in the innate immune response. LCN2 significantly decreased in the cerebrospinal...

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Detalles Bibliográficos
Autores principales: Pinyopornpanish, Kanokporn, Phrommintikul, Arintaya, Angkurawaranon, Chaisiri, Kumfu, Sirinart, Chattipakorn, Nipon, Chattipakorn, Siriporn C
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8089985/
http://dx.doi.org/10.1210/jendso/bvab048.858
Descripción
Sumario:Introduction: Metabolic syndrome (MetS) is associated with an increased risk of cognitive impairment. Lipocalin-2 (LCN2) or neutrophil gelatinase-associated lipocalin (NGAL), is an inflammatory protein, and participates in the innate immune response. LCN2 significantly decreased in the cerebrospinal fluid of individuals with mild cognitive impairment. A recent study reported that circulating lipocalin-2 is involved in early AD pathogenesis. However, the association of LCN2 and cognition in MetS patients are still unclear. Then, the present study aims to evaluate whether serum LCN2 levels are associated with the alteration of cognitive function in MetS subjects. Methods: Participants with MetS, but without dementia or prior psychiatric problems, were enrolled to the study. The demographic data and physical examination were assembled. Blood samples were collected to evaluate the metabolic parameters. Levels of serum LCN2 were determined with ELISA assay. The global score of the Thai version of Montreal cognitive assessment (MoCA) was used to assess cognitive function. Multivariable regression analysis was used to determine the associations. Results: Among 202 MetS participants, 111 (54.95 %) were female, and average age was 64.6 (SD 8.6). Mean serum LCN2 and MoCA score were 30.7 ng/ml (SD 17.6) and 19.3 (SD 4.8), respectively. Serum LCN2 levels were negatively associated with the MoCA scores in crude analysis (B=-0.053; 95%CI -0.090, -0.015; p 0.006). After adjustment for sex, age, waist circumference, and creatinine levels, there was an association between the higher serum LCN2 levels and the lower MoCA scores (B=-0.049; 95%CI -0.090, -0.008; p 0.019). Conclusion: These findings suggest the association between serum LCN2 levels and MCI in MetS subjects. However, further longitudinal study should be investigated to support the link between serum LCN2 levels and cognitive impairment.