Panic disorder is one of the chronic and disabling anxiety disorders. There has been evidence for either genetic heterogeneity or complex inheritance, with environmental factor interactions and multiple single genes, in panic disorder's etiology. Linkage studies have implicated several chromosomal regions, but no research has replicated evidence for major genes involved in panic disorder. Researchers have suggested several neurotransmitter systems are related to panic disorder. However, to date no candidate gene association studies have established specific loci. Recently, researchers have emphasized genome-wide association studies. Results of two genome-wide association studies on panic disorder failed to show significant associations. Evidence exists for differences regarding gender and ethnicity in panic disorder. Increasing evidence suggests genes underlying panic disorder overlap, transcending current diagnostic boundaries. In addition, an anxious temperament and anxiety-related personality traits may represent intermediate phenotypes that predispose to panic disorder. Future research should focus on broad phenotypes, defined by comorbidity or intermediate phenotypes. Genome-wide association studies in large samples, studies of gene-gene and gene-environment interactions, and pharmacogenetic studies are needed.
This contribution aims to integrate findings of our recently reported three brain imaging studies on young narcolepsy-cataplexy patients [1][2][3]. All brain images were acquired using 3.0 Tesla MRI. In our prior study of a voxel-based morphometry [1], narcoleptic patients showed gray matter (GM) deficits in the hypothalamus and fronto-limbic areas. Hypothalamic GM deficits correlated with severity of narcolepsy. In our diffusion tensor imaging study that assessed global white matter (WM) integrity [2], narcoleptic patients had decreased WM integrity especially in fronto-limbic areas, which were associated with sleepiness and attention deficit. Prefrontal metabolite concentration was measured in a proton magnetic resonance spectroscopy [3]. Narcoleptic patients had higher GABA levels in the medial prefrontal areas. This is potentially related to the compensation of nocturnal sleep disturbance. Hypothalamus seems to be a key structure in narcoleptic symptoms. However, both GM and WM abnormalities of fronto-limbic areas were also related to narcolepsy and its symptoms. Compensatory alteration of GABA was also found in the areas. Taken together, our reports suggest that fronto-limbic area, as well as hypothalamus, may be implicated in narcolepsy. References[1] Gray matter deficits in young adults with narcolepsy. Acta Neurol Scand 2009;119:61-7. [2] Decreased fractional anisotropy values in brains of young narcoleptic patients. 2009; presented in APSS. [3] Increased GABA levels in medial prefrontal cortex of young adults with narcolepsy.Two types of monoamine oxidase (MAO), type A (MAO-A) and type B (MAO-B), have been identified. Generally, MAO-A is highly expressed in noradrenergic/adrenergic neurons such as the locus coeruleus, whereas MAO-B is highly expressed in serotonergic and histaminergic neurons and distinct populations of glia such as tanicytes. On the other hand, it has been reported that non-catecholaminergic neurons also express MAOs in an adult rat brain. Extracellular serotonin (5-HT), norepinephrine / epinephrine (NE/E), and dopamine (DA) appear to be removed by a reuptake mechanism; subsequently, they are metabolized by intracellular MAO activity. In the hypothalamus, 5-HT and DBHpositive varicosities densely distribute around hypothalamic nucleus, likely MAO activity affecting the neuronal functions. In the present study, we investigated the distribution of MAOs and the anatomical relation to the neuropeptide-expressing neurons in the rat hypothalamus. We performed enzyme histochemistry for MAO-A or MAO-B, and use specific antibodies for MAO-A and MAO-B. In the result, we found moderate MAO-A enzyme activities in the distinct neuronal populations, and strong MAO-B activity in some glial cells including tanicytes. MAO-A-immunoreactivities (IR) were found in the varicosities of noradrenergic/adrenergic neurons and in the cell bodies of some neuropeptides-expressing neurons in the lateral hypothalamus. Especially, orexin neurons robustly express MAO-A, but not MAO-B. Objective:We have elucidated the p...
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