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Herbal Medicine for Anxiety, Depression and Insomnia. Current neuropharmacology The prevalence and comorbidity of psychiatric disorders such as depression, anxiety and insomnia are very common. These well-known forms of psychiatric disorders have been affecting many people from all around the world. Herb alone, as well as herbal formula, is commonly prescribed for the therapies of mental illnesses. Since various adverse events of western medication exist, the number of people who use herbs to benefit their health is increasing. Over the past decades, the exploration in the area of herbal psychopharmacology has received much attention. Literatures showed a variety of herbal mechanisms of action used for the therapy of depression, anxiety and insomnia, involving reuptake of monoamines, affecting neuroreceptor binding and channel transporter activity, modulating neuronal communication or hypothalamic-pituitary adrenal axis (HPA) etc. Nonetheless, a systematic review on herbal pharmacology in depression, anxiety and insomnia is still lacking. This review has been performed to further identify modes of action of different herbal medicine, and thus provides useful information for the application of herbal medicine. 10.2174/1570159x1304150831122734
Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants. Nature medicine Depression is a common, devastating illness. Current pharmacotherapies help many patients, but high rates of a partial response or no response, and the delayed onset of the effects of antidepressant therapies, leave many patients inadequately treated. However, new insights into the neurobiology of stress and human mood disorders have shed light on mechanisms underlying the vulnerability of individuals to depression and have pointed to novel antidepressants. Environmental events and other risk factors contribute to depression through converging molecular and cellular mechanisms that disrupt neuronal function and morphology, resulting in dysfunction of the circuitry that is essential for mood regulation and cognitive function. Although current antidepressants, such as serotonin-reuptake inhibitors, produce subtle changes that take effect in weeks or months, it has recently been shown that treatment with new agents results in an improvement in mood ratings within hours of dosing patients who are resistant to typical antidepressants. Within a similar time scale, these new agents have also been shown to reverse the synaptic deficits caused by stress. 10.1038/nm.4050
Rheumatoid arthritis and depression: an inflammatory perspective. Nerurkar Louis,Siebert Stefan,McInnes Iain B,Cavanagh Jonathan The lancet. Psychiatry The coexistence of immune-mediated inflammatory diseases with depression has long been recognised. Data that illustrate the intimate associations between peripheral and brain immune responses raise the possibility of shared pathophysiological mechanisms. These associations include the negative effects of proinflammatory cytokines on monoaminergic neurotransmission, neurotrophic factors, and measures of synaptic plasticity. The evidence supporting this association is accumulating and includes findings from clinical trials of immunomodulatory therapy, indicating that these interventions can provide benefits to mental health independent of improvements in physical disease scores. In this Review, we assess this evidence in relation to rheumatoid arthritis and depression, with a focus on innate immune and molecular responses to inflammation, and discuss the challenges of assessing causation in this population, acknowledging the difficulty of assessing the confounding and contributory effects of pain and fatigue. We also discuss how future clinical and preclinical research might improve diagnosis of depression in people with rheumatoid arthritis and shed light on mechanisms that could be substrates for therapeutic interventions. 10.1016/S2215-0366(18)30255-4
Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential. Signal transduction and targeted therapy Major depressive disorder (MDD) is a chronic, generally episodic and debilitating disease that affects an estimated 300 million people worldwide, but its pathogenesis is poorly understood. The heritability estimate of MDD is 30-40%, suggesting that genetics alone do not account for most of the risk of major depression. Another factor known to associate with MDD involves environmental stressors such as childhood adversity and recent life stress. Recent studies have emerged to show that the biological impact of environmental factors in MDD and other stress-related disorders is mediated by a variety of epigenetic modifications. These epigenetic modification alterations contribute to abnormal neuroendocrine responses, neuroplasticity impairment, neurotransmission and neuroglia dysfunction, which are involved in the pathophysiology of MDD. Furthermore, epigenetic marks have been associated with the diagnosis and treatment of MDD. The evaluation of epigenetic modifications holds promise for further understanding of the heterogeneous etiology and complex phenotypes of MDD, and may identify new therapeutic targets. Here, we review preclinical and clinical epigenetic findings, including DNA methylation, histone modification, noncoding RNA, RNA modification, and chromatin remodeling factor in MDD. In addition, we elaborate on the contribution of these epigenetic mechanisms to the pathological trait variability in depression and discuss how such mechanisms can be exploited for therapeutic purposes. 10.1038/s41392-023-01519-z
Altered Connectivity in Depression: GABA and Glutamate Neurotransmitter Deficits and Reversal by Novel Treatments. Neuron The mechanisms underlying the pathophysiology and treatment of depression and stress-related disorders remain unclear, but studies in depressed patients and rodent models are beginning to yield promising insights. These studies demonstrate that depression and chronic stress exposure cause atrophy of neurons in cortical and limbic brain regions implicated in depression, and brain imaging studies demonstrate altered connectivity and network function in the brains of depressed patients. Studies of the neurobiological basis of the these alterations have focused on both the principle, excitatory glutamate neurons, as well as inhibitory GABA interneurons. They demonstrate structural, functional, and neurochemical deficits in both major neuronal types that could lead to degradation of signal integrity in cortical and hippocampal regions. The molecular mechanisms underlying these changes have not been identified but are thought to be related to stress induced excitotoxic effects in combination with elevated adrenal glucocorticoids and inflammatory cytokines as well as other environmental factors. Transcriptomic studies are beginning to demonstrate important sex differences and, together with genomic studies, are starting to reveal mechanistic domains of overlap and uniqueness with regards to risk and pathophysiological mechanisms with schizophrenia and bipolar disorder. These studies also implicate GABA and glutamate dysfunction as well as immunologic mechanisms. While current antidepressants have significant time lag and efficacy limitations, new rapid-acting agents that target the glutamate and GABA systems address these issues and offer superior therapeutic interventions for this widespread and debilitating disorder. 10.1016/j.neuron.2019.03.013
Roles of olfactory system dysfunction in depression. Yuan Ti-Fei,Slotnick Burton M Progress in neuro-psychopharmacology & biological psychiatry The olfactory system is involved in sensory functions, emotional regulation and memory formation. Olfactory bulbectomy in rat has been employed as an animal model of depression for antidepressant discovery studies for many years. Olfaction is impaired in animals suffering from chronic stress, and patients with clinical depression were reported to have decreased olfactory function. It is believed that the neurobiological bases of depression might include dysfunction in the olfactory system. Further, brain stimulation, including nasal based drug delivery could provide novel therapies for management of depression. 10.1016/j.pnpbp.2014.05.013
Olfactory markers of depression and Alzheimer's disease. Marine Naudin,Boriana Atanasova Neuroscience and biobehavioral reviews Depression and Alzheimer's disease are two common and closely intertwined diseases in the elderly. Bio-markers for their early diagnosis would be helpful for clinicians. The brain areas involved in depression, Alzheimer's disease and in olfactory processing overlap, leading to suggestions that olfaction could constitute a potential marker of these diseases. Here, we review the literature in the relevant clinical and olfactory fields, and consider which olfactory measures and factors could serve as markers of these diseases. It has been reported repeatedly that there is an alteration of odor identification in Alzheimer's disease but not in depression. These observations provide strong arguments that this olfactory marker may serve as a complementary tool for the early screening of patients. Odor threshold detection and odor hedonic aspect may constitute complementary markers of the efficacy of depression therapy. However, there are numerous contradictory data and innovative methods are required to investigate whether investigations of olfaction can usefully contribute to routine clinical practice. 10.1016/j.neubiorev.2014.06.016
Symptoms of depression change with olfactory function. Scientific reports Olfactory loss is associated with symptoms of depression. The present study, conducted on a large cohort of mostly dysosmic patients, aimed to investigate whether improvement in olfactory performance would correspond with a decrease in depression severity. In 171 participants (157 dysosmic), we assessed olfactory function and severity of depression before and after an average interval of 11 months, with many patients showing improvement in olfactory function. Separate analyses were conducted for (a) the whole group of patients and (b) the group of dysosmic patients using both classic and Bayesian approaches. For odor identification, Student t test demonstrated that the whole sample improved consistently, especially within the group of dysosmic patients. The dysosmic group also improved in odor threshold and overall olfactory function. Pearson correlation showed that an increase in olfactory function was associated with a decrease in depression severity, particularly in dysosmic patients. To conclude, the present results indicate that symptoms of depression change with olfactory function in general and odor identification in particular. 10.1038/s41598-022-09650-7
Impaired Subcortical Detection of Auditory Changes in Schizophrenia but Not in Major Depression. Gaebler Arnim Johannes,Zweerings Jana,Koten Jan Willem,König Andrea Anna,Turetsky Bruce I,Zvyagintsev Mikhail,Mathiak Klaus Schizophrenia bulletin The mismatch negativity is a cortical response to auditory changes and its reduction is a consistent finding in schizophrenia. Recent evidence revealed that the human brain detects auditory changes already at subcortical stages of the auditory pathway. This finding, however, raises the question where in the auditory hierarchy the schizophrenic deficit first evolves and whether the well-known cortical deficit may be a consequence of dysfunction at lower hierarchical levels. Finally, it should be resolved whether mismatch profiles differ between schizophrenia and affective disorders which exhibit auditory processing deficits as well. We used functional magnetic resonance imaging to assess auditory mismatch processing in 29 patients with schizophrenia, 27 patients with major depression, and 31 healthy control subjects. Analysis included whole-brain activation, region of interest, path and connectivity analysis. In schizophrenia, mismatch deficits emerged at all stages of the auditory pathway including the inferior colliculus, thalamus, auditory, and prefrontal cortex. In depression, deficits were observed in the prefrontal cortex only. Path analysis revealed that activation deficits propagated from subcortical to cortical nodes in a feed-forward mechanism. Finally, both patient groups exhibited reduced connectivity along this processing stream. Auditory mismatch impairments in schizophrenia already manifest at the subcortical level. Moreover, subcortical deficits contribute to the well-known cortical deficits and show specificity for schizophrenia. In contrast, depression is associated with cortical dysfunction only. Hence, schizophrenia and major depression exhibit different neural profiles of sensory processing deficits. Our findings add to a converging body of evidence for brainstem and thalamic dysfunction as a hallmark of schizophrenia. 10.1093/schbul/sbz027
Auditory selective attention in adolescents with major depression: An event-related potential study. Greimel E,Trinkl M,Bartling J,Bakos S,Grossheinrich N,Schulte-Körne G Journal of affective disorders BACKGROUND:Major depression (MD) is associated with deficits in selective attention. Previous studies in adults with MD using event-related potentials (ERPs) reported abnormalities in the neurophysiological correlates of auditory selective attention. However, it is yet unclear whether these findings can be generalized to MD in adolescence. Thus, the aim of the present ERP study was to explore the neural mechanisms of auditory selective attention in adolescents with MD. METHODS:24 male and female unmedicated adolescents with MD and 21 control subjects were included in the study. ERPs were collected during an auditory oddball paradigm. RESULTS:Depressive adolescents tended to show a longer N100 latency to target and non-target tones. Moreover, MD subjects showed a prolonged latency of the P200 component to targets. Across groups, longer P200 latency was associated with a decreased tendency of disinhibited behavior as assessed by a behavioral questionnaire. LIMITATIONS:To be able to draw more precise conclusions about differences between the neural bases of selective attention in adolescents vs. adults with MD, future studies should include both age groups and apply the same experimental setting across all subjects. CONCLUSIONS:The study provides strong support for abnormalities in the neurophysiolgical bases of selective attention in adolecents with MD at early stages of auditory information processing. Absent group differences in later ERP components reflecting voluntary attentional processes stand in contrast to results reported in adults with MD and may suggest that adolescents with MD possess mechanisms to compensate for abnormalities in the early stages of selective attention. 10.1016/j.jad.2014.10.022
Olfaction as a marker for depression. Croy Ilona,Hummel Thomas Journal of neurology Olfactory and emotional higher processing pathways share common anatomical substrates. Hence, depression is often accompanied by alterations in olfactory function. These alterations are negative in nature and may involve decreased activation in olfactory eloquent structures or decreased volume in the olfactory bulb (OB). We suggest that olfaction and depression interact in two ways. First, olfactory function in depression is impaired as a consequence of reduced olfactory attention and diminished olfactory receptor turnover rates. Second, the OB may constitute a marker for enhanced vulnerability to depression. Closer analysis of these interactions may help to explain observed experimental data, as well as to elucidate new therapeutic strategies involving olfaction. Because of the difficulties to disentangle cause from consequence in the relationship between olfaction and depression, longitudinal and intervention studies are necessary to elucidate this further. 10.1007/s00415-016-8227-8
Taste and smell perception in depression. Amsterdam J D,Settle R G,Doty R L,Abelman E,Winokur A Biological psychiatry
To smell autoimmunity: anti-P-ribosomal autoantibodies, depression, and the olfactory system. Shoenfeld Yehuda Journal of autoimmunity Central Nervous System involvement in Systemic Lupus Erythematosus (CNS-SLE) is very common and ranges between 25%-70% of the patients. The CNS involvement is listed in the ARA criteria for SLE diagnosis. CNS-SLE is associated with more than 20 different autoantibodies. Yet, remarkable among them are the anti-P-ribosomal antibodies (anti-PR). These autoantibodies directed mainly against the carboxy 22 amino acids of the PO, P1 P2 ribosomal phosphoproteins. They are capable of penetrating lived cells and inducing apoptotic changes as well as leading to inhibition of specific cytokine secretion. The titer of the autoantibodies correlate with disease activity, kidney involvement and hepatitis. In this review, the mechanisms involved in CNS involvement and its relationship with anti-P ribosomal antibodies will be described. 10.1016/j.jaut.2007.02.012