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P2‐287: A δ HOMOLOG FOR DEMENTIA CASE FINDING WITH REPLICATION IN ADNI
Author(s) -
Royall Donald R.,
Bishnoi Ram J.,
Palmer Raymond F.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.976
Subject(s) - dementia , clinical dementia rating , latent variable , structural equation modeling , psychology , confirmatory factor analysis , metric (unit) , neuroimaging , replication (statistics) , disease , audiology , clinical psychology , medicine , neuroscience , computer science , artificial intelligence , machine learning , operations management , virology , economics
tertiles. Cox proportional hazard models were used to determine the predictive value of nutritional markers. All models were corrected for sex, age, BMI, history of cardiovascular disease and lipid lowering medication. Results: Twenty-one (20%) SCD patients and 43 (33%)MCI patients showed progression toMCI or dementia during follow-up. Vitamin B6, betaine and HDL cholesterol in blood, and homocysteine in CSF were associated with clinical progression in the SCD group (p for trend <0.05). Low levels of vitamin B6, betaine and HDL cholesterol and high levels of CSF homocysteine were protective for progression ((HR 95%CI1⁄4 3.9 (1.0-14.6), 4.4 (1.1-17.3), 6.0 (1.2-30.6), 0.3 (0.1-1.0), highest vs. lowest tertile). Within the MCI group only CSF S-adenosylmethionine was associated with clinical progression (p for trend ˂0.05), high levels were protective for progression to dementia (HR 95% CI1⁄4 0.4(0.2-1.0), highest vs. lowest tertile). Conclusions: In this large panel of nutritional markers we found subtle associations between various nutritional markers and clinical progression. In contrast to previous studies, higher HDL cholesterol levels and lower homocysteine levels were associated with an increased risk on clinical progression. The mild alterations shown here might reflect early metabolic changes prior to clinical progression. More distinct change in nutritional status and metabolism found in dementia patients is perhaps a consequence rather than a cause of cognitive impairment.