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Divergent Roles of APOAI and APOM in the Identification of Alcohol Use Disorder and their Association with Inflammation and Cognitive Decline: A Pilot Study.
International Journal of Neuropsychopharmacology 2024 July 6
BACKGROUND: Alcohol Use Disorder (AUD) courses with inflammation and cognitive decline. Apolipoproteins have emerged as novel target compounds related to inflammatory processes and cognition.
METHODS: A cross-sectional study was performed on abstinent AUD patients with at least one month of abstinence (n=33; 72.7% men) and healthy controls (n=34; 47.1% men). A battery of plasma apolipoproteins (APOAI, APOAII, APOB, APOCII, APOE, APOJ and APOM), plasma inflammatory markers (LPS, LBP), and their influence on cognition and presence of the disorder were investigated.
RESULTS: Higher levels of plasma APOAI, APOB, APOE and APOJ, as well as the proinflammatory LPS, were observed in the AUD group, irrespective of sex, whereas APOM levels were lower versus controls. Hierarchical logistic regression analyses, adjusting for covariates (age, sex, education), associated APOM with the absence of cognitive impairment in AUD, and identified APOAI and APOM as strong predictors of the presence or absence of the disorder, respectively. APOAI and APOM did not correlate with alcohol abuse variables or liver status markers but they showed an opposite profile in their associations with LPS (positive for APOAI; negative for APOM) and cognition (negative for APOAI; positive for APOM) in the entire sample.
CONCLUSIONS: The HDL constituents APOAI and APOM were differentially regulated in the plasma of AUD subjects compared to controls, playing divergent roles in the disorder identification and associations with inflammation and cognitive decline.
METHODS: A cross-sectional study was performed on abstinent AUD patients with at least one month of abstinence (n=33; 72.7% men) and healthy controls (n=34; 47.1% men). A battery of plasma apolipoproteins (APOAI, APOAII, APOB, APOCII, APOE, APOJ and APOM), plasma inflammatory markers (LPS, LBP), and their influence on cognition and presence of the disorder were investigated.
RESULTS: Higher levels of plasma APOAI, APOB, APOE and APOJ, as well as the proinflammatory LPS, were observed in the AUD group, irrespective of sex, whereas APOM levels were lower versus controls. Hierarchical logistic regression analyses, adjusting for covariates (age, sex, education), associated APOM with the absence of cognitive impairment in AUD, and identified APOAI and APOM as strong predictors of the presence or absence of the disorder, respectively. APOAI and APOM did not correlate with alcohol abuse variables or liver status markers but they showed an opposite profile in their associations with LPS (positive for APOAI; negative for APOM) and cognition (negative for APOAI; positive for APOM) in the entire sample.
CONCLUSIONS: The HDL constituents APOAI and APOM were differentially regulated in the plasma of AUD subjects compared to controls, playing divergent roles in the disorder identification and associations with inflammation and cognitive decline.
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