Brain-Derived Neurotrophic Fac

Objective: The Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene is associated with geriatric depression. In studies of younger adults without depression, met allele carriers exhibit smaller hippocampal volumes and have poorer performance on neuropsychological tests. The authors examined the relationship between the BDNF gene and hippocampal volumes in depressed and nondepressed older individuals and its relationship with memory functions mediated by the hippocampus. Design: One hundred seventy-six elderly depressed white participants and 88 nondepressed participants completed clinical assessments, neuropsychological testing, and provided blood samples for genotyping. One hundred seventy-three participants also underwent brain magnetic resonance imaging. Statistical modeling tested the relationship between genotype and hippocampal volume and function while controlling for diagnosis and other covariates. Results: BDNF genotype was not associated with a difference in performance on tests mediated by the hippocampus, including word list learning, prose recall, nonverbal memory, or digit span. After controlling for covariates, BDNF genotype was not significantly associated with hippocampal volume (F^sub [1, 171]^ = 1.10, p = 0.30). Conclusion: Despite different findings in younger populations, the BDNF Val66Met polymorphism is not significantly associated with hippocampal volume or function in a geriatric population. The authors hypothesize that other factors may have a stronger effect on hippocampal structure in older individuals and that the association between the Val66Met polymorphism and geriatric depression is mediated through other mechanisms. (Am J Geriatr Psychiatry 2010; 18:323-331)

Amplifier LD-AM-24-X

Key Words: makeup brush Genetic polymorphism, MRI, depression, hippocampus

The etiology of depression remains unexplained. In general, depression may be driven by altered neural and emotional response to environmental stimuli, coupled with decreased ability to regulate that emotional response. Neuroimaging studies have revealed structural1 and functional2 differences between depressed and normal populations. This work is accompanied by studies investigating contributing factors at the molecular level, such as the neurotrophic model of depression,3 and research at the genetic level that has identified single nucleotide polymorphisms (SNPs) that may be linked with vulnerability to depression.3,4 Because none of these elements on their own has provided a comprehensive understanding of the pathophysiology of depression, exploration of the interplay among neuroanatomic, molecular, and genetic factors might be a more productive approach.

Depressed individuals exhibit smaller hippocampal volumes, when compared with nondepressed individuals,5 a finding also observed in elderly populations,6 although not always replicated.7,8 Smaller hippocampal volumes in depressed subjects are associated as adverse antidepressant outcomes including a failure to remit9'10 and greater likelihood of relapse.11 It is possible that genetic differences may explain part of the discrepancy in results of studies exarrtining hippocampal volume in depression. One potentially important contributor is the valine (val) to methionine (met) substitution in the 5' proregion of the human brain-derived neurotrophic factor (BDNF) protein, a result of a functional SNP (Val66Met). The met allele is more common in late-life depression (LLD)12,13 and is associated with smaller hippocampal volumes in healthy adults.14 Studies that have examined the association between the BDNF genotype and hippocampal volumes in major depression among younger adult
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