General Psychiatry Review - 4.28.12
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via psychiatric journal articles - Google News on 4/26/12
New Psychiatry Research Released Scoop.co.nz (press release) The latest issue of Australasian Psychiatry has been released and contains a number of highly interesting articles pertaining to various aspects of the field. These include: • Mental health planning for children and youth: is it developmentally ... and more » |
via psychiatric diagnosis - Google News on 4/28/12
Army warns doctors against using certain drugs in PTSD treatment // April 25, 2012 Nextgov An April 10 policy memo that the Army Medical Command released regarding the diagnosis and treatment of PTSD said a class of drugs known as benzodiazepines, which include Xanax and Valium, could intensify rather than reduce combat stress symptoms and ... |
via international psychiatry - Google News on 4/28/12
Suicides have Greeks on edge before election WXEL Attempted suicides and demand for psychiatric help has risen as Greece struggles to cope with the worst economic crisis since World War Two. Nikiforos Angelopoulos, a professor of psychiatry, has a busy psychotherapy practice in an upmarket Athens ... and more » |
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Pers Soc Psychol Bull. 2012 Apr 24;
Authors: Feeney BC, Lemay EP
Abstract
In this article, a Theory of Emotional Capital is investigated, which stipulates that relationships are able to withstand threats when partners have built “emotional capital” within the relationship (by contributing to positive, shared experiences). Support for this idea was obtained in two studies using two samples (newlywed couples and more established married couples) and two methodologies (daily diary and observational methods). Both studies showed that individuals with high emotional capital were less reactive to relationship threats than those with low emotional capital. The importance of emotional capital for healthy and stable relationships is discussed.
PMID: 22535924 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Pers Soc Psychol Bull. 2012 Apr 24;
Authors: Guo T, Ji LJ, Spina R, Zhang Z
Abstract
This article examines cultural differences in how people value future and past events. Throughout four studies, the authors found that European Canadians attached more monetary value to an event in the future than to an identical event in the past, whereas Chinese and Chinese Canadians placed more monetary value to a past event than to an identical future event. The authors also showed that temporal focus-thinking about the past or future-explained cultural influences on the temporal value asymmetry effect. Specifically, when induced to think about and focus on the future, Chinese valued the future more than the past, just like Euro-Canadians; when induced to think about and focus on the past, Euro-Canadians valued the past more than the future, just like Chinese.
PMID: 22535925 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 16;
Authors: Elsayed M, Banasr M, Duric V, Fournier NM, Licznerski P, Duman RS
Abstract
BACKGROUND: Basic and clinical studies report that the expression of fibroblast growth factor-2 (FGF-2) is decreased in the prefrontal cortex (PFC) of depressed subjects or rodents exposed to stress and increased following antidepressant treatment. Here, we aim to determine if 1) FGF-2/fibroblast growth factor receptor (FGFR) signaling is sufficient and required for mediating an antidepressant response behaviorally and cellularly; and 2) if the antidepressant actions of FGF-2 are mediated specifically by the PFC. METHODS: The role of FGF-2 signaling in behavioral models of depression and anxiety was tested using chronic unpredictable stress (CUS)/sucrose consumption test (SCT), forced swim test (FST), and novelty suppressed feeding test (NSFT). We also assessed the number of bromodeoxyuridine labeled dividing glial cells in the PFC as a cellular index relevant to depression (i.e., decreased by stress and increased by antidepressant treatment). RESULTS: Chronic FGF-2 infusions (intracerebroventricular) blocked the deficit in SCT caused by CUS. Moreover, the response to antidepressant treatment in the CUS/SCT and FST was abolished upon administration of an inhibitor of FGFR activity, SU5402. These results are consistent with the regulation of proliferating cells in the PFC, a portion of which are of oligodendrocyte lineage. Lastly, subchronic infusions of FGF-2 into the PFC but not into the dorsal striatum produced antidepressant-like and anxiolytic-like effects on FST and NSFT respectively. CONCLUSIONS: These findings demonstrate that FGF-2/FGFR signaling is sufficient and necessary for the behavioral, as well as gliogenic, actions of antidepressants and highlight the PFC as a brain region sensitive to the antidepressant actions of FGF-2.
PMID: 22513055 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 18;
Authors: Zarate CA, Brutsche N, Laje G, Luckenbaugh DA, Venkata SL, Ramamoorthy A, Moaddel R, Wainer IW
Abstract
BACKGROUND: Ketamine has rapid antidepressant effects lasting as long as 1 week in patients with major depressive disorder (MDD) and bipolar depression (BD). Ketamine is extensively metabolized. This study examined the relationship between ketamine metabolites and response, diagnosis, and psychotomimetic symptoms in MDD and BD patients. METHODS: Following a 40-minute ketamine infusion (.5 mg/kg), plasma samples were collected at 40, 80, 110, and 230 minutes and day 1 postinfusion in 67 patients currently experiencing a major depressive episode (MDD, n = 45; BD, n = 22). Concentrations of ketamine, norketamine (NK), dehydronorketamine (DHNK), six hydroxynorketamine metabolites (HNK), and hydroxyketamine (HK) were measured. Plasma concentrations were analyzed by diagnostic group and correlated with patients’ depressive, psychotic, and dissociative symptoms. The relationship between cytochrome P450 gene polymorphisms and metabolites, response, and diagnosis was also examined. RESULTS: Ketamine, NK, DHNK, four of six HNKs, and HK were present during the first 230 minutes postinfusion. Patients with BD had higher plasma concentrations of DHNK, (2S,6S;2R,6R)-HNK, (2S,6R;2R,6S)-HNK, and (2S,5S;2R,5R)-HNK than patients with MDD, who, in turn, had higher concentrations of (2S,6S;2R,6R)-HK. Higher (2S,5S;2R,5R)-HNK concentrations were associated with nonresponse to ketamine in BD patients. Dehydronorketamine, HNK4c, and HNK4f levels were significantly negatively correlated with psychotic and dissociative symptoms at 40 minutes. No relationship was found between cytochrome P450 genes and any of the parameters examined. CONCLUSIONS: A diagnostic difference was observed in the metabolism and disposition of ketamine. Concentrations of (2S,5S;2R,5R)-HNK were related to nonresponse to ketamine in BD. Some hydroxylated metabolites of ketamine correlated with psychotic and dissociative symptoms.
PMID: 22516044 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 19;
Authors: Monterosso J, Piray P, Luo S
Abstract
We review the key findings in the application of neuroeconomics to the study of addiction. Although there are not “bright line” boundaries between neuroeconomics and other areas of behavioral science, neuroeconomics coheres around the topic of the neural representations of “Value” (synonymous with the “decision utility” of behavioral economics). Neuroeconomics parameterizes distinct features of Valuation, going beyond the general construct of “reward sensitivity” widely used in addiction research. We argue that its modeling refinements might facilitate the identification of neural substrates that contribute to addiction. We highlight two areas of neuroeconomics that have been particularly productive. The first is research on neural correlates of delay discounting (reduced Valuation of rewards as a function of their delay). The second is work that models how Value is learned as a function of “prediction-error” signaling. Although both areas are part of the neuroeconomic program, delay discounting research grows directly out of behavioral economics, whereas prediction-error work is grounded in models of learning. We also consider efforts to apply neuroeconomics to the study of self-control and discuss challenges for this area. We argue that neuroeconomic work has the potential to generate breakthrough research in addiction science.
PMID: 22520343 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 May 15;71(10):842-3
Authors: Dayan P, Walton ME
PMID: 22520727 [PubMed - in process]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 May 15;71(10):844-5
Authors: Bullmore E
PMID: 22520728 [PubMed - in process]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 18;
Authors: Han S, Yang BZ, Kranzler HR, Oslin D, Anton R, Farrer LA, Gelernter J
Abstract
BACKGROUND: A genetic contribution to cannabis dependence (CaD) has been established but susceptibility genes for CaD remain largely unknown. METHODS: We employed a multistage design to identify genetic variants underlying CaD. We first performed a genome-wide linkage scan for CaD in 384 African American (AA) and 354 European American families ascertained for genetic studies of cocaine and opioid dependence. We then conducted association analysis under the linkage peak, first using data from a genome-wide association study from the Study of Addiction: Genetics and Environment, followed by replication studies of prioritized single nucleotide polymorphisms (SNPs) in independent samples. RESULTS: We identified the strongest linkage evidence with CaD (logarithm of odds = 2.9) on chromosome 8p21.1 in AAs. In the association analysis of the Study of Addiction: Genetics and Environment sample under the linkage peak, we identified one SNP (rs17664708) associated with CaD in both AAs (odds ratio [OR] = 2.93, p = .0022) and European Americans (OR = 1.38, p = .02). This SNP, located at NRG1, a susceptibility gene for schizophrenia, was prioritized for further study. We replicated the association of rs17664708 with CaD in an independent AAs sample (OR = 2.81, p = .0068). The joint analysis of the two AA samples demonstrated highly significant association between rs17664708 and CaD with adjustment for either global (p = .00044) or local ancestry (p = .00075). CONCLUSIONS: Our study shows that NRG1 is probably a susceptibility gene for CaD, based on convergent evidence of linkage and replicated associations in two independent AA samples.
PMID: 22520967 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 18;
Authors: Lubke GH, Hottenga JJ, Walters R, Laurin C, de Geus EJ, Willemsen G, Smit JH, Middeldorp CM, Penninx BW, Vink JM, Boomsma DI
Abstract
Genome-wide association studies of psychiatric disorders have been criticized for their lack of explaining a considerable proportion of the heritability established in twin and family studies. Genome-wide association studies of major depressive disorder in particular have so far been unsuccessful in detecting genome-wide significant single nucleotide polymorphisms (SNPs). Using two recently proposed methods designed to estimate the heritability of a phenotype that is attributable to genome-wide SNPs, we show that SNPs on current platforms contain substantial information concerning the additive genetic variance of major depressive disorder. To assess the consistency of these two methods, we analyzed four other complex phenotypes from different domains. The pattern of results is consistent with estimates of heritability obtained in twin studies carried out in the same population.
PMID: 22520966 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 20;
Authors: Spencer SJ, Xu L, Clarke MA, Lemus M, Reichenbach A, Geenen B, Kozicz T, Andrews ZB
Abstract
BACKGROUND: Ghrelin plays important roles in glucose metabolism, appetite, and body weight regulation, and recent evidence suggests ghrelin prevents excessive anxiety under conditions of chronic stress. METHODS: We used ghrelin knockout (ghr-/-) mice to examine the role of endogenous ghrelin in anxious behavior and hypothalamic-pituitary-adrenal axis (HPA) responses to acute stress. RESULTS: Ghr-/- mice are more anxious after acute restraint stress, compared with wild-type (WT) mice, with three independent behavioral tests. Acute restraint stress exacerbated neuronal activation in the hypothalamic paraventricular nucleus and medial nucleus of the amygdala in ghr-/- mice compared with WT, and exogenous ghrelin reversed this effect. Acute stress increased neuronal activation in the centrally projecting Edinger-Westphal nucleus in WT but not ghr-/- mice. Ghr-/- mice exhibited a lower corticosterone response after stress, suggesting dysfunctional glucocorticoid negative feedback in the absence of ghrelin. We found no differences in dexamethasone-induced Fos expression between ghr-/- and WT mice, suggesting central feedback was not impaired. Adrenocorticotropic hormone replacement elevated plasma corticosterone in ghr-/-, compared with WT mice, indicating increased adrenal sensitivity. The adrenocorticotropic hormone response to acute stress was significantly reduced in ghr-/- mice, compared with control subjects. Pro-opiomelanocortin anterior pituitary cells express significant growth hormone secretagogue receptor. CONCLUSIONS: Ghrelin reduces anxiety after acute stress by stimulating the HPA axis at the level of the anterior pituitary. A novel neuronal growth hormone secretagogue receptor circuit involving urocortin 1 neurons in the centrally projecting Edinger-Westphal nucleus promotes an appropriate stress response. Thus, ghrelin regulates acute stress and offers potential therapeutic efficacy in human mood and stress disorders.
PMID: 22521145 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 20;
Authors: Tang AC, Reeb-Sutherland BC, Romeo RD, McEwen BS
Abstract
BACKGROUND: Behavioral inhibition (BI) to novelty is thought to be a stable temperament type that appears early in life and is a major risk factor for anxiety disorders. In the rat, habituation of such inhibition can be facilitated via neonatal novelty exposure (NNE), thus reducing BI to novelty. Here, we tested the hypothesis that this early intervention effect is modulated by the context of maternal self-stress regulation. METHODS: The NNE was carried out during postnatal days 1-21, in which one half of each litter was exposed to a relatively novel nonhome environment for 3-min daily while the remaining one half stayed in the home cage. After weaning, BI to novelty was assessed in an open field with a measure of disinhibition defined as a greater increase in exploration across two brief trials. Maternal context was characterized by trait measures of hypothalamic-pituitary-adrenal (HPA) axis reactivity, including basal and stress-evoked corticosterone (CORT) responses. RESULTS: Family-to-family variations in the NNE effect were associated with variations in maternal HPA function-a low-basal CORT and high-evoked CORT response profile constituting the context for a novelty-induced facilitation of disinhibition (i.e., a greater increase in exploratory activity over repeated trials) and an opposite HPA profile constituting the context for a novelty-induced reduction of disinhibition. CONCLUSIONS: This result is consistent with the hypothesis that maternal self-stress regulation modulates the effect of early life intervention on BI to novelty and suggests that effective interventions should include strategies to help mothers improve their self-stress regulation.
PMID: 22521147 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 20;
Authors: Roberts AL, Galea S, Austin SB, Cerda M, Wright RJ, Rich-Edwards JW, Koenen KC
Abstract
BACKGROUND: Research conducted using small samples of persons exposed to extreme stressors has documented an association between parental and offspring posttraumatic stress disorder (PTSD), but it is unknown whether this association exists in the general population and whether trauma exposure mediates this association. We sought to determine whether mothers’ posttraumatic stress symptoms were associated with PTSD in their young adult children and whether this association was mediated by higher trauma exposure in children of women with PTSD. METHODS: Using data from a cohort of mothers (n = 6924) and a cohort of their children (n = 8453), we calculated risk ratios (RR) for child’s PTSD and examined mediation by trauma exposure. RESULTS: Mother’s lifetime posttraumatic stress symptoms were associated with child’s PTSD in dose-response fashion (mother’s 1-3 symptoms, child’s RR = 1.2; mother’s 4-5 symptoms, RR = 1.3; mother’s 6-7 symptoms, RR = 1.6, compared with children of mothers with no symptoms, p < .001 for each). Mother’s lifetime symptoms were also associated with child’s trauma exposure in dose-response fashion. Elevated exposure to trauma substantially mediated elevated risk for PTSD in children of women with symptoms (mediation proportion, 74%, p < .001). CONCLUSIONS: Intergenerational association of PTSD is clearly present in a large population-based sample. Children of women who had PTSD were more likely than children of women without PTSD to experience traumatic events; this suggests, in part, why the disorder is associated across generations. Health care providers who treat mothers with PTSD should be aware of the higher risk for trauma exposure and PTSD in their children.
PMID: 22521146 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 20;
Authors: Cornwell BR, Salvadore G, Furey M, Marquardt CA, Brutsche NE, Grillon C, Zarate CA
Abstract
BACKGROUND: Clinical evidence that ketamine, a nonselective N-methyl-D-aspartate receptor (NMDAR) antagonist, has therapeutic effects within hours in people suffering from depression suggests that modulating glutamatergic neurotransmission is a fundamental step in alleviating the debilitating symptoms of mood disorders. Acutely, ketamine increases extracellular glutamate levels, neuronal excitability, and spontaneous γ oscillations, but it is unknown whether these effects are key to the mechanism of antidepressant action of ketamine. METHODS: Twenty drug-free major depressive disorder patients received a single, open-label intravenous infusion of ketamine hydrochloride (.5 mg/kg). Magnetoencephalographic recordings were made approximately 3 days before and approximately 6.5 hours after the infusion, whereas patients passively received tactile stimulation to the right and left index fingers and also while they rested (eyes-closed). Antidepressant response was assessed by percentage change in Montgomery-Åsberg Depression Rating Scale scores. RESULTS: Patients with robust improvements in depressive symptoms 230 min after infusion (responders) exhibited increased cortical excitability within this antidepressant response window. Specifically, we found that stimulus-evoked somatosensory cortical responses increase after infusion, relative to pretreatment responses in responders but not in treatment nonresponders. Spontaneous somatosensory cortical γ-band activity during rest did not change within the same timeframe after ketamine in either responders or nonresponders. CONCLUSIONS: These findings suggest NMDAR antagonism does not lead directly to increased cortical excitability hours later and thus might not be sufficient for therapeutic effects of ketamine to take hold. Rather, increased cortical excitability as depressive symptoms improve is consistent with the hypothesis that enhanced non-NMDAR-mediated glutamatergic neurotransmission via synaptic potentiation is central to the antidepressant effect of ketamine.
PMID: 22521148 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 20;
Authors: Bagot RC, Tse YC, Nguyen HB, Wong AS, Meaney MJ, Wong TP
Abstract
BACKGROUND: Variations in maternal care in the rat associate with robust differences in hippocampal development and synaptic plasticity in the offspring. Maternal care also influences pituitary-adrenal stress responses and corticosterone (CORT) regulation of hippocampal plasticity. N-methyl-D-aspartate receptors (NMDAR) regulate synaptic plasticity, and NMDAR function is modulated by stress and CORT. We hypothesized that altered NMDAR function underlies the interaction of maternal and stress effects on hippocampal synaptic plasticity. METHODS: We used electrophysiology and western blot to examine NMDAR synaptic function/expression and NMDAR-dependent long-term potentiation (LTP) in adult offspring of mothers that varied in the frequency of pup licking/grooming (LG) (i.e., High or Low LG). RESULTS: Basal NMDAR synaptic function was enhanced in the hippocampal dentate gyrus (DG) of adult Low LG offspring. Synaptic expression of NMDAR but not α-amino-3-hydroxy-methyl-4-isoxazole propionic acid receptors was also increased. Stress level CORT (100 nmol/L) rapidly (<20 min) and robustly increased NMDAR function in High LG offspring, eliminating the maternal effect. Corticosterone did not affect NMDAR function in Low LG offspring. Bovine serum albumin-conjugated CORT reproduced the CORT effect in High LG offspring, implicating a membrane-bound corticosteroid receptor. NMDAR hyperfunction might impair synaptic plasticity. Partial NMDAR antagonism by low concentration DL-2-Amino-5-phosphonopentanoic acid rescued a basal LTP deficit in Low LG offspring and inhibited LTP in High LG offspring. CONCLUSIONS: Low LG offspring exhibit basally elevated NMDAR function coupled with insensitivity to CORT modulation indicative of a chronic alteration of NMDAR function. Elevated NMDAR function in the hippocampus might underlie impaired LTP in Low LG offspring.
PMID: 22521150 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 20;
Authors: Kawakami N, Abdulghani EA, Alonso J, Bromet EJ, Bruffaerts R, Caldas-de-Almeida JM, Chiu WT, de Girolamo G, de Graaf R, Fayyad J, Ferry F, Florescu S, Gureje O, Hu C, Lakoma MD, Leblanc W, Lee S, Levinson D, Malhotra S, Matschinger H, Medina-Mora ME, Nakamura Y, Oakley Browne MA, Okoliyski M, Posada-Villa J, Sampson NA, Viana MC, Kessler RC
Abstract
BACKGROUND: Better information on the human capital costs of early-onset mental disorders could increase sensitivity of policy makers to the value of expanding initiatives for early detection and treatment. Data are presented on one important aspect of these costs: the associations of early-onset mental disorders with adult household income. METHODS: Data come from the World Health Organization (WHO) World Mental Health Surveys in 11 high-income, five upper-middle income, and six low/lower-middle income countries. Information about 15 lifetime DSM-IV mental disorders as of age of completing education, retrospectively assessed with the WHO Composite International Diagnostic Interview, was used to predict current household income among respondents aged 18 to 64 (n = 37,741) controlling for level of education. Gross associations were decomposed to evaluate mediating effects through major components of household income. RESULTS: Early-onset mental disorders are associated with significantly reduced household income in high and upper-middle income countries but not low/lower-middle income countries, with associations consistently stronger among women than men. Total associations are largely due to low personal earnings (increased unemployment, decreased earnings among the employed) and spouse earnings (decreased probabilities of marriage and, if married, spouse employment and low earnings of employed spouses). Individual-level effect sizes are equivalent to 16% to 33% of median within-country household income, and population-level effect sizes are in the range 1.0% to 1.4% of gross household income. CONCLUSIONS: Early mental disorders are associated with substantial decrements in income net of education at both individual and societal levels. Policy makers should take these associations into consideration in making health care research and treatment resource allocation decisions.
PMID: 22521149 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 23;
Authors: Nikolova YS, Bogdan R, Brigidi BD, Hariri AR
Abstract
BACKGROUND: Stressful life events are among the most reliable precipitants of major depressive disorder; yet, not everyone exposed to stress develops depression. It has been hypothesized that robust neural reactivity to reward and associated stable levels of positive affect (PA) may protect against major depressive disorder in the context of environmental adversity. However, little empirical data exist to confirm this postulation. Here, we test the hypothesis that individuals with relatively low ventral striatum (VS) reactivity to reward will show low PA levels in the context of recent life stress, while those with relatively high VS reactivity will be protected against these potentially depressogenic effects. METHODS: Differential VS reactivity to positive feedback was assessed using blood oxygen level-dependent functional magnetic resonance imaging in a sample of 200 nonpatient young adults. Recent life stress, current depressive symptoms, and PA were assessed via self-report. Linear regression models were used to investigate the moderating effects of VS reactivity on the relationship between recent stress and state PA across participants. RESULTS: Recent life stress interacted with VS reactivity to predict self-reported state PA, such that higher levels of life stress were associated with lower PA for participants with relatively low, but not for those with high, VS reactivity. These effects were independent of age, gender, race/ethnicity, trait PA, and early childhood trauma. CONCLUSIONS: The current results provide empirical evidence for the potentially protective role of robust reward-related neural responsiveness against reductions in PA that may occur in the wake of life stress and possibly vulnerability to depression precipitated by stressful life events.
PMID: 22534456 [PubMed - as supplied by publisher]
via Medicine JournalFeeds » Psychiatry by admin on 4/27/12
Biol Psychiatry. 2012 Apr 23;
Authors: Meier S, Demirakca T, Brusniak W, Wolf I, Liebsch K, Tunc-Skarka N, Nieratschker V, Witt SH, Matthäus F, Ende G, Flor H, Rietschel M, Diener C, Schulze TG
Abstract
BACKGROUND: The aging of the human brain is accompanied by changes in cortical structure as well as functional activity and variable degrees of cognitive decline. One-third of the observable inter-individual differences in cognitive decline are thought to be heritable. SCN1A encodes the sodium channel α subunit and is considered to be a susceptibility gene for several neurological disorders with prominent cognitive deficits. In a recent genome-wide association study the C allele of the SCN1A variant rs10930201 was observed to be significantly associated with poor short-term memory performance. rs10930201 was further observed to be related to differences in neural activity during a working memory task. METHODS: The aim of the present study was to explore whether SCN1A modifies the vulnerability to aging processes of the human brain. Therefore we assessed the interacting effects of the SCN1A vulnerability allele rs10930201 and age in terms of brain activity and brain morphology in 62 healthy volunteers between 21 and 82 years of age. RESULTS: In C allele carriers, activity in the right inferior frontal cortex and the posterior cingulate cortex increased with age. Moreover, exploratory analysis revealed regional effects of rs10930201 on brain structure, indicating reduced gray matter densities in the frontal and insular regions in the C allele carriers. CONCLUSIONS: Collectively, the present results suggest that the SCN1A polymorphism has modulatory effects on brain morphology and vulnerability to age-related alterations in brain activity of cortical regions that subserve working memory.
PMID: 22534457 [PubMed - as supplied by publisher]
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