Current Issue : April - June Volume : 2013 Issue Number : 2 Articles : 7 Articles
Consistent evidence links major depression and its affective components to negative health outcomes. Although\r\nthe pathways of these effects are likely complex and multifactorial, recent evidence suggests that innate\r\ninflammatory processes may play a role. An overview of current literature suggests that pathways between\r\nnegative moods and inflammation are bi-directional. Indeed, negative moods activate peripheral physiologic\r\nmechanisms that result in an up regulation of systemic levels of inflammation. Conversely, peripheral inflammatory\r\nmediators signal the brain to affect behavioral, affective and cognitive changes that are consistent with symptoms\r\nof major depressive disorder. It is likely that these pathways are part of a complex feedback loop that involves the\r\nnervous, endocrine, and immune systems and plays a role in the modulation of peripheral inflammatory responses\r\nto central and peripheral stimuli, in central responses to peripheral immune activation and in the maintenance of\r\nhomeostatic balance. Further research is warranted to fully understand the role of central processes in this\r\nfeedback loop, which likely contributes to the pathophysiology of mental and physical health...
Background: Potassium channels have been proposed to play a role in mechanisms of neural plasticity, and the\r\nKv4.2 subunit has been implicated in the regulation of action-potential back-propagation to the dendrites.\r\nAlterations in mechanisms of plasticity have been further proposed to underlie various psychiatric disorders, but\r\nthe role of Kv4.2 in anxiety or depression is not well understood.\r\nMethods: In this paper, we analyzed the phenotype Kv4.2 knockout mice based on their neurological function, on\r\na battery of behaviors including those related to anxiety and depression, and on plasticity-related learning tasks.\r\nResults: We found a novelty-induced hyperactive phenotype in knockout mice, and these mice also displayed\r\nincreased reactivity to novel stimulus such as an auditory tone. No clear anxiety- or depression-related phenotype\r\nwas observed, nor any alterations in learning/plasticity-based paradigms.\r\nConclusions: We did not find clear evidence for an involvement of Kv4.2 in neuropsychiatric or plasticity-related\r\nphenotypes, but there was support for a role in Kv4.2 in dampening excitatory responses to novel stimuli....
Neurosteroids are synthesized in the brain and modulate brain excitability. There is increasing evidence of their\r\nsedative, anesthetic and antiseizure properties, as well as their influence on mood. Currently neurosteroids are\r\nclassified as pregnane neurosteroids (allopregnanolone and allotetrahydrodeoxycorticosterone), androstane\r\nneurosteroids (androstanediol and etiocholanone) or sulfated neurosteroids (pregnenolone sulfate and\r\ndehydroepiandrosterone sulfate). Both preclinical and clinical findings indicate that progesterone derivative\r\nneurosteroids such as allopregnanolone and allotetrahydrodeoxycorticosterone play a role in mood disorders.\r\nClozapine and olanzapine, which were shown to be effective in stabilizing bipolar disorder, elevate pregnenolone\r\nlevels in rat hippocampus, cerebral cortex, and serum. In lithium-treated mice, the blood levels of allopregnanolone\r\nand pregnenolone were elevated compared to control levels. Women diagnosed with bipolar disorder typically\r\nshow symptomatic exacerbation in relation to the menstrual cycle, and show vulnerability to the onset or\r\nrecurrence of mood disorders immediately after giving birth, when the levels of neurosteroid derivatives of\r\nprogesterone drop. Whereas in women who had recovered from bipolar disorder, the plasma concentration of\r\nallopregnanolone was elevated compared to either healthy controls or women with major depressive disorder\r\nduring the premenstrual period. During depressive episodes, blood level of allopregnanolone is low. Treatment\r\nwith fluoxetine tends to stabilize the levels of neurosteroids in depression. These findings converge to suggest that\r\nthese steroids have significant mood-stabilizing effect. This hypothesis is consistent with the observation that a\r\nnumber of anticonvulsants are effective therapies for bipolar disorder, a finding also consistent with the antiseizure\r\nproperties of neurosteroids. Further exploration of action of neuroactive steroids is likely to open new frontiers in\r\nthe investigation of the etiology and treatment of mood disorders, particularly bipolar disorders....
Background: Neuropsychiatric symptoms such as psychosis are prevalent in patients with probable Alzheimer�s\r\ndisease (AD) and are associated with increased morbidity and mortality. Because these disabling symptoms are\r\ngenerally not well tolerated by caregivers, patients with these symptoms tend to be institutionalized earlier than\r\npatients without them. The identification of protective and risk factors for neuropsychiatric symptoms in AD would\r\nfacilitate the development of more specific treatments for these symptoms and thereby decrease morbidity and\r\nmortality in AD. The E4 allele of the apolipoprotein E (APOE) gene is a well-documented risk factor for the\r\ndevelopment of AD. However, genetic association studies of the APOE 4 allele and BPS in AD have produced\r\nconflicting findings.\r\nMethods: This study investigates the association between APOE and neuropsychiatric symptoms in a large sample\r\nof clinically well-characterized subjects with probable AD (n=790) who were systematically evaluated using the\r\nConsortium to Establish a Registry for Alzheimer�s Disease (CERAD) Behavioral Rating Scale for Dementia (BRSD).\r\nResults: Our study found that hallucinations were significantly more likely to occur in subjects with no APO?4\r\nalleles than in subjects with two ?4 alleles (15% of subjects and 5% of subjects, respectively; p=.0066), whereas\r\nthere was no association between the occurrence of delusions, aberrant motor behavior, or agitation and the\r\nnumber of ?4 alleles. However, 94% of the subjects with hallucinations also had delusions (D+H).\r\nConclusion: These findings suggest that in AD the ?4 allele is differentially associated with D+H but not delusions\r\nalone. This is consistent with the hypothesis that distinct psychotic subphenotypes may be associated with the\r\nAPOE allele....
The number of neuroimaging studies has grown exponentially in recent years and their results are not always\r\nconsistent. Meta-analyses are helpful to summarize this vast literature and also offer insights that are not apparent\r\nfrom the individual studies. In this review, we describe the main methods used for meta-analyzing neuroimaging\r\ndata, with special emphasis on their relative advantages and disadvantages. We describe and discuss metaanalytical\r\nmethods for global brain volumes, methods based on regions of interest, label-based reviews, voxelbased\r\nmeta-analytic methods and online databases. Regions of interest-based methods allow for optimal statistical\r\nanalyses but are affected by a limited and potentially biased inclusion of brain regions, whilst voxel-based methods\r\nbenefit from a more exhaustive and unbiased inclusion of studies but are statistically more limited. There are also\r\nrelevant differences between the different available voxel-based meta-analytic methods, and the field is rapidly\r\nevolving to develop more accurate and robust methods. We suggest that in any meta-analysis of neuroimaging\r\ndata, authors should aim to: only include studies exploring the whole brain; ensure that the same threshold\r\nthroughout the whole brain is used within each included study; and explore the robustness of the findings via\r\ncomplementary analyses to minimize the risk of false positives....
Background: Among the most robust neural abnormalities differentiating individuals with Attention-Deficit/\r\nHyperactivity Disorder (ADHD) from typically developing controls are elevated levels of slow oscillatory activity\r\n(e.g., theta) and reduced fast oscillatory activity (e.g., alpha and beta) during resting-state electroencephalography\r\n(EEG). However, studies of resting state EEG in adults with ADHD are scarce and yield inconsistent findings.\r\nMethods: EEG profiles, recorded during a resting-state with eyes-open and eyes-closed conditions, were compared\r\nfor college students with ADHD (n = 18) and a nonclinical comparison group (n = 17).\r\nResults: The ADHD group showed decreased power for fast frequencies, especially alpha. This group also showed\r\nincreased power in the slow frequency bands, however, these effects were strongest using relative power\r\ncomputations. Furthermore, the theta/beta ratio measure was reliably higher for the ADHD group. All effects were\r\nmore pronounced for the eyes-closed compared to the eyes-open condition. Measures of intra-individual variability\r\nsuggested that brains of the ADHD group were less variable than those of controls.\r\nConclusions: The findings of this pilot study reveal that college students with ADHD show a distinct neural pattern\r\nduring resting state, suggesting that oscillatory power, especially alpha, is a useful index for reflecting differences in\r\nneural communication of ADHD in early adulthood....
Convergent data from rodents and human studies have led to the development of models describing the neural\r\nmechanisms of fear extinction. Key components of the now well-characterized fear extinction network include the\r\namygdala, hippocampus, and medial prefrontal cortical regions. These models are fueling novel hypotheses that\r\nare currently being tested with much refined experimental tools to examine the interactions within this network.\r\nLagging far behind, however, is the examination of sex differences in this network and how sex hormones\r\ninfluence the functional activity and reactivity of these brain regions in the context of fear inhibition. Indeed, there\r\nis a large body of literature suggesting that sex hormones, such as estrogen, do modulate neural plasticity within\r\nthe fear extinction network, especially in the hippocampus.\r\nAfter a brief overview of the fear extinction network, we summarize what is currently known about sex differences\r\nin fear extinction and the influence of gonadal hormones on the fear extinction network. We then go on to\r\npropose possible mechanisms by which sex hormones, such as estrogen, may influence neural plasticity within the\r\nfear extinction network. We end with a discussion of how knowledge to be gained from developing this line of\r\nresearch may have significant ramifications towards the etiology, epidemiology and treatment of anxiety disordes....
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