Benzodiazepines (BDZ), which potentiate the action of GABA at four subtypes of GABA<sub>A</sub> receptors (α1, α2, α3, and α5GABA<sub>A</sub>Rs), are highly effective against anxiety disorders, but also cause severe side effects greatly limiting their clinical application.
The ABCB1 genotypes of rs1922242 (P=0.0028) and rs1202184 (P=0.0021) showed significant association with the severity of depressive symptoms as assessed by the Hamilton Rating Scale for Depression adjusted with Hamilton Rating Scale for Anxiety.
Our findings demonstrate that the ACC and vHPC regulate fear expressed in novel, nonthreatening environments via projections to the BLA but do so as a result of training intensity or time, respectively.<b>SIGNIFICANCE STATEMENT</b> Anxiety disorders are characterized by a common symptom that promotes overgeneralization of fear in nonthreatening environments.
Moreover, we investigated neural activity that mediates 5-HTTLPR association with RRS by scanning short-short (s/s) and long-long (l/l) homozygotes of 5-HTTLPR, using functional MRI, during a Cyberball game that resulted in social exclusion. l/l compared with s/s allele carriers reported higher RRS but lower social interaction anxiety. l/l compared with s/s carriers showed stronger activity in the right ventral prefrontal cortex (RVPFC) and stronger functional connectivity between the dorsal and rostral ACC when being excluded from the Cyberball game.
Interestingly, we observed distinct patterns of anxiety differences in amygdala-rostral ACC connectivity and subjective fear ratings depending on harsh parenting levels, suggesting a history of harsh parenting is linked with unique neural and behavioral anxious manifestations, which are different from anxiety manifestations in a context of low adversity.
The main goal of this systematic literature review was summarize the evidence on the utilization and effectiveness of treatments for depression and anxiety in persons with IBD.
In regression analysis at baseline, the IPQ-R domain of greater perception of a cyclical nature of IBD was an independent predictor of anxiety, and a greater perceived emotional impact of IBD was an independent predictor of anxiety, depression, and HRQoL.
Anxiety and depression are associated with lower cognitive function in MS, with a similar pattern observed in persons with other IMID, including IBD and RA, and persons without an IMID.
Based on the results of this study, the IBD-SAS displayed adequate psychometric properties and can meaningfully contribute to the assessment of IBD-specific anxiety in adolescents diagnosed with IBD, thus filling an empirical and clinical need in this population.
When compared with placebo or other antihypertensive medications, AT1R blockers and angiotensin converting enzyme inhibitors were associated with improved overall quality of life (standard mean difference = 0.11, 95% confidence interval = [0.08, 0.14], p < 0.0001), positive wellbeing (standard mean difference = 0.11, 95% confidence interval = [0.05, 0.17], p < 0.0001), mental (standard mean difference = 0.15, 95% confidence interval = [0.06, 0.25], p < 0.0001), and anxiety (standard mean difference = 0.08, 95% confidence interval = [0.01, 0.16], p < 0.0001) domains of QoL.
Individuals in the ≥4 ACEs group endorsed more intense creative experiences compared to the no-ACE and 1-3 ACEs groups (p = .006, η<sup>2</sup> = .048); however, in the third MANCOVA they had heightened anxiety, internalized shame, dissociative processing, emotion-oriented coping, and cumulative trauma (p < .001, η<sup>2</sup> = .132).
First, our study verifies the ameliorative effects of donepezil on behavioral deficits in both working memory and anxiety in APP/PS1 double transgenic mice, at a time point that AChE is not inhibited.
Accumulating evidence from mouse models points to the G protein-coupled receptor RGS2 (regulator of G-protein signaling 2) as a promising candidate gene for anxiety in humans.
Since central administration of neuropeptide S (NPS) has been shown to exert anxiolytic effects on rodent behavior in a number of studies, genetic variants of its cognate G-protein coupled receptor (NPSR1) became the focus of several recent human studies on anxiety and anxiety disorders.
The G protein-coupled receptor neuropeptide S receptor 1 (NPSR1) and its ligand neuropeptide S (NPS) form a signaling system mainly implicated in susceptibility to asthma and inflammatory disorders in humans and regulation of anxiety and arousal in rodents.
Significant improvement was observed in memory, orientation, depression and anxiety (HAD scale) in both mild and moderate cases; in anxiety (NPI scale) in mild cases; and in delirium, hallucinations, agitation, irritability, and language disorders in the group with moderate Alzheimer disease.
Epigenetic and/or genetic variation in the gene encoding the receptor for adenylate-cyclase activating polypeptide 1 (ADCYAP1R1) has been linked to post-traumatic stress disorder in adults and anxiety in children.
Further integration of epigenetic data and gene × environment interaction are promising approaches, as highlighted by FKPB5 and PACAP, early life trauma and stress-related anxiety disorders.
Pituitary adenylate cyclase activating polypeptide (PACAP, <i>Adcyap1</i>) is a neuromodulator implicated in anxiety, metabolism and reproductive behavior.