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MS and cognition and APOE - The ongoing conundrum about biomarkers

Neurology (Impact Factor: 8.3). 02/2008; 70(3):164-5. DOI: 10.1212/01.wnl.0000297938.22145.a7
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    • "However, there usually lacks robust interpretation of the cognitive impairment in MS in most studies, which can either be only a symptom on account of myelin damage and axonal loss, suggesting the severity of the disease, or be at a subclinical stage of neurodegenerative diseases such as Alzheimer's disease, irrelevant of the disease of MS per se. Hence findings, either positive or negative, must be interpreted with caution [115]. Anyway, cognitive impairment in newly diagnosed MS is intriguing, since it may be of help to evaluate the disease. "
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    ABSTRACT: The role of apolipoprotein E (ApoE) alleles has received recent attention in depressive disorders, the ApoE epsilon4 conferring greater risk for poorer outcomes, and the ApoE epsilon2 allele providing some protective effects. Depression is common in multiple sclerosis (MS) and the role of ApoE alleles is unknown. To evaluate ApoE alleles in relation to symptoms of depression in a cohort of patients with MS participating in the Sonya Slifka Longitudinal Multiple Sclerosis Study (Slifka Study). To examine risk and protection, depressed mood and positive affect were each investigated with respect to the ApoE epsilon4 and ApoE epsilon2 alleles, respectively. Of the total 101 participants, 22.8% were ApoE epsilon2 carriers and 21.8% were ApoE epsilon4 carriers. Hierarchical linear regression analyses suggested that after controlling for demographics, disease duration, and disability, ApoE epsilon2 significantly predicted increased positive affect (R2Delta=0.05, F(1,94)=5.44, P=0.02) and was associated with decreased severity of depressive symptoms, although this did not reach statistical significance (R2Delta=0.03, F(1,94)=3.44, P=0.06). ApoE epsilon4 did not significantly predict depression status. The presence of the ApoE epsilon2 allele in this study is suggested to be protective against depressive symptoms in our subsample of patients recruited from the Slifka Study. These findings are consistent with reports in psychiatric populations linking ApoE epsilon2 with decreased incidence of depressive disorders. Further investigation would be warranted to understand the role of ApoE genotypes and risk for depressive symptoms.
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