Ann Clin Psychiatry. 2012 Feb; 24(1): 91-109
Ramasubbu R, Taylor VH, Saaman Z, Sockalingham S, Li M, Patten S, Rodin G, Schaffer A, Beaulieu S, McIntyre RS

Medical comorbidity in patients with mood disorders has become an increasingly important clinical and global public health issue. Several specific medical conditions are associated with an increased risk of mood disorders, and conversely, mood disorders are associated with increased morbidity and mortality in patients with specific medical disorders.To help understand the bidirectional relationship and to provide an evidence-based framework to guide the treatment of mood disorders that are comorbid with medical illness, we have reviewed relevant articles and reviews published in English-language databases (to April 2011) on the links between mood disorders and several common medical conditions, evaluating the efficacy and safety of pharmacologic and psychosocial treatments. The medical disorders most commonly encountered in adult populations (ie, cardiovascular disease, cerebrovascular disease, cancer, human immunodeficiency virus, hepatitis C virus, migraine, multiple sclerosis, epilepsy, and osteoporosis) were chosen as the focus of this review.Emerging evidence suggests that depression comorbid with several medical disorders is treatable and failure to treat depression in medically ill patients may have a negative effect on medical outcomes.This review summarizes the available evidence and provides treatment recommendations for the management of comorbid depression in medically ill patients.

Ann Clin Psychiatry. 2012 Feb; 24(1): 82-90
Ramasubbu R, Beaulieu S, Taylor VH, Schaffer A, McIntyre RS

Medical comorbidity is commonly encountered in individuals with major depressive disorder (MDD) and bipolar disorder (BD). The presence of medical comorbidity has diagnostic, prognostic, treatment, and etiologic implications underscoring the importance of timely detection and treatment.A selective review of relevant articles and reviews published in English-language databases (1968 to April 2011) was conducted. Studies describing epidemiology, temporality of onset, treatment implications, and prognosis were selected for review.A growing body of evidence from epidemiologic, clinical, and biologic studies suggests that the relationship between medical illness and mood disorder is bidirectional in nature. It provides support for the multiplay of shared and specific etiologic factors interlinking these conditions.This article describes the complex interactions between medical illness and mood disorders and provides a meaningful approach to their comorbid clinical diagnosis and management.

PLoS Negl Trop Dis. 2012 Jan; 6(1): e1493
Wallin MT, Pretell EJ, Bustos JA, Caballero M, Alfaro M, Kane R, Wilken J, Sullivan C, Fratto T, Garcia HH

Few studies have focused on the cognitive morbidity of neurocysticercosis (NCC), one of the most common parasitic infections of the central nervous system. We longitudinally assessed the cognitive status and quality of life (QoL) of patients with incident symptomatic NCC cases and matched controls.The setting of the study was the Sabogal Hospital and Cysticercosis Unit, Department of Transmissible Diseases, National Institute of Neurological Sciences, Lima, Peru. The design was a longitudinal study of new onset NCC cases and controls. Participants included a total of 14 patients with recently diagnosed NCC along with 14 healthy neighborhood controls and 7 recently diagnosed epilepsy controls. A standardized neuropsychological battery was performed at baseline and at 6 months on NCC cases and controls. A brain MRI was performed in patients with NCC at baseline and 6 months. Neuropsychological results were compared between NCC cases and controls at both time points. At baseline, patients with NCC had lower scores on attention tasks (p<0.04) compared with epilepsy controls but no significant differences compared to healthy controls. Six months after receiving anti-parasitic treatment, the NCC group significantly improved on tasks involving psychomotor speed (p<0.02). QoL at baseline suggested impaired mental function and social function in both the NCC and epilepsy group compared with healthy controls. QoL gains in social function (p = 0.006) were noted at 6 months in patients with NCC.Newly diagnosed patients with NCC in this sample had mild cognitive deficits and more marked decreases in quality of life at baseline compared with controls. Improvements were found in both cognitive status and quality of life in patients with NCC after treatment.

PLoS One. 2012; 7(1): e30855
Stachowiak B, Weingartl HM

Nipah virus (NiV), a zoonotic paramyxovirus, is highly contagious in swine, and can cause fatal infections in humans following transmission from the swine host. The main viral targets in both species are the respiratory and central nervous systems, with viremia implicated as a mode of dissemination of NiV throughout the host. The presented work focused on the role of peripheral blood mononuclear cells (PBMC) in the viremic spread of the virus in the swine host. B lymphocytes, CD4-CD8-, as well as CD4+CD8- T lymphocytes were not permissive to NiV, and expansion of the CD4+CD8- cells early post infection was consistent with functional humoral response to NiV infection observed in swine. In contrast, significant drop in the CD4+CD8- T cell frequency was observed in piglets which succumbed to the experimental infection, supporting the hypothesis that antibody development is the critical component of the protective immune response. Productive viral replication was detected in monocytes, CD6+CD8+ T lymphocytes and NK cells by recovery of infectious virus in the cell supernatants. Virus replication was supported by detection of the structural N and the non-structural C proteins or by detection of genomic RNA increase in the infected cells. Infection of T cells carrying CD6 marker, a strong ligand for the activated leukocyte cell adhesion molecule ALCAM (CD166) highly expressed on the microvascular endothelial cell of the blood-air and the blood-brain barrier may explain NiV preferential tropism for small blood vessels of the lung and brain.

PLoS One. 2012; 7(1):
Devine MJ, Kaganovich A, Ryten M, Mamais A, Trabzuni D, Manzoni C, McGoldrick P, Chan D, Dillman A, Zerle J, Horan S, Taanman JW, Hardy J, Marti-Masso JF, Healy D, Schapira AH, Wolozin B, Bandopadhyay R, Cookson MR, van der Brug MP, Lewis PA

[This corrects the article on p. e22489 in vol. 6.].

PLoS One. 2012; 7(1):
Erblich B, Zhu L, Etgen AM, Dobrenis K, Pollard JW

[This corrects the article on p. e26317 in vol. 6.].

Front Genet. 2011; 2: 111
Brigati C, Saccuman MC, Banelli B, Di Vinci A, Casciano I, Borzì L, Forlani A, Allemanni G, Romani M

We are transient beings, in a world of constantly changing culture. At home in the fields of Art and Science, seemingly capable of magnificent abstractions, humans have an intense need to externalize their insights. Music is an art and a highly transmissible cultural product, but we still have an incomplete understanding of how our musical experience shapes and is vividly retained within our brain, and how it affects our behavior. However, the developing field of social epigenetics is now helping us to describe how communication and emotion, prime hallmarks of music, can be linked to a transmissible, biochemical change.

Front Genet. 2011; 2: 89
Davies W

Technological advances and a greater degree of inter-laboratory co-operation mean that genome-wide analyses can now be used to identify genetic variants that are robustly associated with the risk of developing psychiatric and neurological disorders. In contrast to the candidate gene approach, such screens may identify variants within genes which have a hitherto unappreciated role in disorder pathogenesis, and whose brain function is obscure. In this Perspective, I discuss how the behavioral functions of such genes may be investigated using model systems, drawing attention to the potential caveats and limitations with such approaches. The power of focused cross-species studies needs to be effectively exploited to enable useful insights into the molecular pathogenesis of common and disabling disorders, and ultimately to provide better clinical outcomes for patients.

Front Genet. 2011; 2: 73
Hibar DP, Kohannim O, Stein JL, Chiang MC, Thompson PM

The quest to identify genes that influence disease is now being extended to find genes that affect biological markers of disease, or endophenotypes. Brain images, in particular, provide exquisitely detailed measures of anatomy, function, and connectivity in the living brain, and have identified characteristic features for many neurological and psychiatric disorders. The emerging field of imaging genomics is discovering important genetic variants associated with brain structure and function, which in turn influence disease risk and fundamental cognitive processes. Statistical approaches for testing genetic associations are not straightforward to apply to brain images because the data in brain images is spatially complex and generally high dimensional. Neuroimaging phenotypes typically include 3D maps across many points in the brain, fiber tracts, shape-based analyses, and connectivity matrices, or networks. These complex data types require new methods for data reduction and joint consideration of the image and the genome. Image-wide, genome-wide searches are now feasible, but they can be greatly empowered by sparse regression or hierarchical clustering methods that isolate promising features, boosting statistical power. Here we review the evolution of statistical approaches to assess genetic influences on the brain. We outline the current state of multivariate statistics in imaging genomics, and future directions, including meta-analysis. We emphasize the power of novel multivariate approaches to discover reliable genetic influences with small effect sizes.

Front Genet. 2011; 2: 68
Jorgensen RA

Front Genet. 2011; 2: 57
Gil-Sánchez A, Demmelmair H, Parrilla JJ, Koletzko B, Larqué E

The concentration of long chain polyunsaturated fatty acid (LCPUFA) in the fetal brain increases dramatically from the third trimester until 18 months of life. Several studies have shown an association between the percentage of maternal plasma docosahexaenoic acid (DHA) during gestation and development of cognitive functions in the neonate. Since only very low levels of LCPUFA are synthesized in the fetus and placenta, their primary source for the fetus is the maternal circulation. Both in vitro and human in vivo studies using labeled fatty acids have shown preferential transfer of LCPUFA from the placenta to the fetus compared with other fatty acids, although the mechanisms involved are still uncertain. The placenta takes up circulating maternal non-esterified fatty acids (NEFA) and fatty acids released mainly by maternal lipoprotein lipase and endothelial lipase. These NEFA may enter the cell by passive diffusion or by means of membrane carrier proteins. Once in the cytosol, NEFA bind to cytosolic fatty acid-binding proteins for transfer to the fetal circulation or can be oxidized within the trophoblasts, and even re-esterified and stored in lipid droplets. Although trophoblast cells are not specialized for lipid storage, LCPUFA may up-regulate peroxisome proliferator activated receptor-γ (PPARγ) and hence the gene expression of fatty acid transport carriers, fatty acid acyl-CoA-synthetases and adipophilin or other enzymes involved in lipolysis, modifying the rate of placental transfer, and metabolism. The placental transfer of LCPUFA during pregnancy seems to be a key factor in the neurological development of the fetus. Increased knowledge of the factors that modify placental transfer of fatty acids would contribute to our understanding of this complex process.

Front Genet. 2011; 2: 16
Zielke LG, Bortfeldt RH, Tetens J, Brockmann GA

The gene encoding the brain-derived neurotrophic factor (BDNF) has been repeatedly associated with human obesity. As such, it could also contribute to the regulation of energy partitioning and the amount of secreted milk fat during lactation, which plays an important role in milk production in dairy cattle. Therefore, we performed an association study using estimated breeding values (EBVs) of bulls and yield deviations of German Holstein dairy cattle to test the effect of BDNF on milk fat yield (FY). A highly significant effect (corrected p-value = 3.362 × 10(-4)) was identified for an SNP 168 kb up-stream of the BDNF transcription start. The association tests provided evidence for an additive allele effect of 5.13 kg of fat per lactation on the EBV for milk FY in bulls and 6.80 kg of fat of the own production performance in cows explaining 1.72 and 0.60% of the phenotypic variance in the analyzed populations, respectively. The analyses of bulls and cows consistently showed three haplotype groups that differed significantly from each other, suggesting at least two different mutations in the BDNF region affecting the milk FY. The FY increasing alleles also had low but significant positive effects on protein and total milk yield which suggests a general role of the BDNF region in energy partitioning, rather than a specific regulation of fat synthesis. The results obtained in dairy cattle suggest similar effects of BDNF on milk composition in other species, including man.