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Psychological Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Harrison Howarth, Jim Bolton, Gary Bell
Acetylcholinesterase inhibitors (donepezil, rivastigmine and galantamine) are recommended in mild to moderate Alzheimer's to improve cognitive function. The N-methyl-D-aspartic acid (NMDA) receptor antagonist memantine is recommended in moderate Alzheimer's intolerant to acetylcholinesterase inhibitors and in severe Alzheimer's. They have a modest effect and should only be started by an experienced specialist.
The Importance of Personalized Nutrition in Psychological Disorders
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Psychogeriatric patients are usually observed to suffer from zinc deficiency (Gronli, Kvamme et al. 2013). Some authors suggested that there is a correlation between the dietary zinc intake and depression; however, this topic is still controversial. According to some studies, zinc intake has a negative correlation with depression, whereas others have shown no correlation at all (Li, Wang et al. 2018). There are some dynamics suggested to convey the association between depression and zinc intake. To begin with, zinc intake regulates the brain’s zinc homeostasis (Takeda, Minami et al. 2001). In addition, neural transmission might be affected by the existence of zinc, such as the activation of N-methyl-D-aspartic acid (NMDA) receptors and the BDNF activity as a common element of depression (Takeda and Tamano 2009; Szewczyk, Kubera et al. 2011; Toth 2011). Moreover, the pathophysiology of depression might be affected by the antioxidant properties of zinc (Swardfager, Herrmann et al. 2013).
Electrical Brain Stimulation to Treat Neurological Disorders
Published in Bahman Zohuri, Patrick J. McDaniel, Electrical Brain Stimulation for the Treatment of Neurological Disorders, 2019
Bahman Zohuri, Patrick J. McDaniel
Studies are being undertaken to modulate the effects of tDCS with various drugs designed to either enhance or suppress the stimulation effects. For example, neuroplasticity after-effects appear to be N-Methyl-D-aspartic acid (NMDA) specific20 as opposed to acute effects;21 therefore, application of tDCS in the presence of NMDA receptor (d-cycloserine, amphetamine) and GABA (lorazepam) agonists have been found to facilitate the aftereffects of tDCS application.22 Targeted therapies wherein pharmacological and electrical stimulation are combined to achieve optimal dose-response relationships in diseases including pain management,23 epilepsy,24 and even Alzheimer’s disease25,26 represent important and exciting areas of future development in brain stimulation.
Homocysteine can aggravate depressive like behaviors in a middle cerebral artery occlusion/reperfusion rat model: a possible role for NMDARs-mediated synaptic alterations
Published in Nutritional Neuroscience, 2023
Mengying Wang, Xiaoshan Liang, Qiang Zhang, Suhui Luo, Huan Liu, Xuan Wang, Na Sai, Xumei Zhang
Abnormalities in neurotransmission via N-methyl-D-aspartic acid receptors (NMDARs) play a role in the pathophysiology of some neuropsychiatric disorders including depression. Both inhibition and stimulation of this receptor convey antidepressant properties [14–16]. The modulation of the NMDAR as a potential therapeutic strategy for major depression is also supported by compelling evidence [17, 18]. Meanwhile, excitotoxicity mediated by NMDARs has been at the center stage of stroke research. It has been reported that cerebral ischemic insult could stimulate NMDARs and triggered calcium influx, eventually induced neuronal death and brain damage [19]. In pre-clinical studies in rats, NMDAR antagonists protected neurons from ischemic death in a model of middle cerebral artery occlusion (MCAO). However, there is limited evidence on the role of NMDAR in PSD. It is well established that HCY activates NMDARs and related intracellular calcium accumulation, inducing neuroexcitatory toxicity [20–22]. Given the NMDAR-modulating role of HCY in the nervous system, we hypothesized that NMDARs involve in the HCY- associated pathogenesis of PSD.
Lack of bombesin receptor-activated protein homologous protein impairs hippocampal synaptic plasticity and promotes chronic unpredictable mild stress induced behavioral changes in mice
Published in Stress, 2023
Xueping Yao, Xiaoqun Qin, Hui Wang, Jiaoyun Zheng, Zhi Peng, Jie Wang, Horst Christian Weber, Rujiao Liu, Wenrui Zhang, Ji Zeng, Suhui Zuo, Hui Chen, Yang Xiang, Chi Liu, Huijun Liu, Lang Pan, Xiangping Qu
PSD95 is one of the major regulators of synaptic maturation and acts as an essential scaffolding protein during synaptogenesis. It was reported to interact, stabilize and help N-methyl-D-aspartic acid receptors (NMDARs) traffic to the postsynaptic membrane and is required for synaptic plasticity associated with NMDA receptor signaling (Chen et al., 2011). No significant loss of PSD95 was observed in hippocampal sections from bc004004−/−mice compared with wild type control mice (Figure 6(A,C)). Western blot analysis of PSD95 in the hippocampal tissues is shown in Figure 6(E,G). Although the main effect of genotype (F (1, 5) = 10.54, p = .02) was significant, further pairwise comparison did not find significant difference on PSD95 expression between knockout mice and control mice. The main effect of CUMS treatment (F (1, 5) = 6.55, p = .05) was not significant and there was no interaction between CUMS treatment and genotype (F (1, 5) = 0.39, p = .56).
The pathological involvement of spinal cord EphB2 in visceral sensitization in male rats
Published in Stress, 2022
Tao Chen, Si Chen, Xuefeng Zheng, Yaofeng Zhu, Ziyun Huang, Linju Jia, Lisi OuYang, Wanlong Lei
Eph receptors are the largest known family of receptor tyrosine kinases (RTKs) (Cisse & Checler, 2015). EphrinB2/EphB2 modulates synaptic plasticity by regulating the function of N-methyl-D-aspartic acid (NMDA) receptors in the post-synaptic membrane. Studies have demonstrated that EphB receptors and their EphrinB ligands are present in laminae I-III of the dorsal horn (Bundesen et al., 2003; Song, Cao, et al., 2008), which distinctly indicates that EphrinB-EphB plays a critical role in the induction and maintenance of neuropathic pain by regulating neural excitability and synaptic activity at the peripheral and central levels (Song, Zheng, et al., 2008; Vasileiou et al., 2013). In addition, EphrinB-EphB molecules contribute to hyperalgesia through the ERK5/CREB pathway (Yu et al., 2017). Therefore the present study aimed to investigate the effects of SPS and EphB2 activation on visceral pain over a time course, and corresponding changes in EphB2 and C-Fos expression in the spinal dorsal horn.