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Mechanism of Action of Isotretinoin
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Isotretinoin-associated depression is a matter of concern and appears to develop in a small subgroup of vulnerable predisposed individuals, particularly those with a personal or family history of mental disorders (111,112). Recent theories for the pathogenesis of depression suggest decreased hippocampal and prefrontal cortex neurogenesis (113–115). Isotretinoin treatment of mice decreased hippocampal neurogenesis and reduced hippocampal volume (116,117). Treatment of hypothalamic cells with 10 μM isotretinoin for 48 h decreased cell growth to 45.6 ± 13% of control (118). Intracerebroventricularly applied ATRA to adult rats increased RAR-α protein expression in the hippocampus and impaired hippocampal neurogenesis correlated with depression-like symptoms (119).
The Influence of Physical Activity on Brain Aging and Cognition: The Role of Cognitive Reserve, Thresholds for Decline, Genetic Influence, and the Investment Hypothesis
Published in James M. Rippe, Lifestyle Medicine, 2019
Maureen K. Kayes, Bradley D. Hatfield
Neurogenesis, the growth of new neurons in the brain, as revealed in the dentate gyrus in animals, represents an exciting finding that holds great promise for medicine since the appearance of new neurons in the human hippocampus—the brain region most affected by AD dementia. This finding suggests resilience to the pathology (i.e., plaques and tangles) through participation in physical activity. In a classic study, van Praag, Kemperman, and Gage6 reported that neurogenesis in adult mice occurred in response to wheel running. After controlling for the effects of environment, they determined that physical activity alone was responsible for the observed proliferation of neurons in the dentate gyrus.6 In addition, van Praag, Christie, Sejnowski, and Gage determined that the appearance of new hippocampal cells in adult mice housed with running wheels was associated with improved cognition, as shown in performance on the Morris Water Maze and enhanced LTP when compared to controls in standard housing.67
Nerve Agent–Induced Seizures and Status Epilepticus: Neuroprotective Strategies
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Frederic Doreu, Karine Thibault, Nina Dupuis
Blocking angiogenesis seemed helpful to prevent the consequences of seizures (Benini et al., 2016). However, things are more complicated, as administration of VEGF was reported to be beneficial in a model of pilocarpine-induced seizures, possibly through an action on astrocytes (Lenzer-Fanara et al., 2017). It was also shown to regulate neurogenesis and to have a beneficial impact on cognition after SE (Han et al., 2017). Studies are lacking in the field of OP poisoning.
Mineralocorticoid receptor agonist aldosterone rescues hippocampal neural stem cell proliferation defects and improves postoperative cognitive function in aged mice
Published in The World Journal of Biological Psychiatry, 2023
Xuhong Fan, Zhenyu Zhao, Zixia Huang, Mingyue Wu, Deming Wang, Ji Xiao
An increasing number of studies have shown that stress, hormones and environmental factors can regulate neurogenesis (Spalding et al. 2013; Aimone et al. 2014). Increased glucocorticoid levels have been shown to reduce progenitor cell proliferation and inhibit hippocampal neurogenesis, and depletion of glucocorticoids by adrenalectomy can reverse this effect (Kim et al. 2004; Garza et al. 2012). Conversely, Overexpression of MR promotes differentiation and survival of embryonic stem cell-derived neurons (Munier et al. 2012). Similarly, forebrain MR overexpression improves memory ability, alleviates anxiety and reduces neuronal loss during cerebral ischaemia in mice (Lai et al. 2007). However, genetic disruption of MR in the hippocampus of adult mice impairs neurogenesis and leads to granule cell degeneration (Gass et al. 2000), and loss of the limbic mineralocorticoid receptor impairs behavioural plasticity (Berger et al. 2006). In addition, aldosterone, the prototypic MR agonist, may promote the proliferation and survival of newly-generated granule cells in the dentate gyrus of adrenalectomized rat (Fischer et al. 2002). Also, the highly potent MR agonist fludrocortisone promotes the survival and proliferation of hippocampal progenitor cells (AHPs) in adult rats (Gesmundo et al. 2016).
Rationale, methods, and progress of the ArthroCaP Study: A prospective cohort study exploring the associations between chronic postsurgical pain and postoperative cognitive dysfunction after elective knee or hip arthroplasty
Published in Canadian Journal of Pain, 2022
Maram Khaled, Jocelyn Kuber, Mary Ferber, Praveen Sritharan, Yarden Levy, Suzanna Becker, Margaret Fahnestock, Meridith Griffin, Kim Madden, Harsha Shanthanna, Maura Marcucci
Numerous studies in animals have linked depression with hippocampal-reduced neurogenesis.33–35 In the absence of a noninvasive measure of neurogenesis in humans, correlational evidence in human studies has identified performance on the MST as putatively neurogenesis sensitive because it is similarly impacted by factors that alter neurogenesis levels in rodents.36,37 Although the contribution of adult neurogenesis to pattern separation remains unclear,38 the hypothesis of a neurogenesis interference as a mechanism through which pain could affect cognition remains plausible and worth further evaluation. Neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1), which support the survival and function of hippocampal cells, are regulators of neurogenesis.39,40 BDNF and IGF-1 have been shown to enhance the association between higher aerobic fitness and better memory performance. Conversely, a reduction in neurotrophic factors might mediate the interaction of pain (and the consequent possible reduction in mobility) or patient satisfaction (as measured by SAPS, which includes also satisfaction with their ability to perform physical tasks) with cognition.
The effects of green tea on cognitive impairments in the rat model of Alzheimer’s disease: protection against inflammatory and oxidative damage
Published in Nutritional Neuroscience, 2022
Mahsa Amirpour, Mohammad Ali Mirshekar, Gohar Sedaghat, Farzaneh Montazerifar, Shadi Shourestani, Saiedeh Arabmoazzen, Mehrdad Naghizadeh
The AD has several causes, of which 1% has been linked to the genetic disorder in the mutation of the genes encoding transmembrane amyloid-protein precursor (APP), or presenilin 1 (PS1) and presenilin 2 (PS2) proteins [48,49]. The decline of soluble APP levels is responsible for the amelioration of impaired cognitive function [50]. The presence of epicatechin in GT can reduce the concentration of presenilin 1 [51]. Also, a study on human tissues found that intracellular Aβ accumulation prior to the growth of extracellular plaques could lead to impaired synapse function and memory impairment [52,53]. The reduction in Aβ production improves neurogenesis in AD patients. Administration of GT, both as an intraperitoneal injection (20 mg/kg) and through drinking water (50 mg/kg), could reduce Aβ levels [54]. The protein tau is a hydrophilic and soluble protein that plays a role in stabilizing microtubules and intercellular transitions [55]. This protein contains an N-terminal, and C-terminal region can be phosphorylated from different locations [56,57]. Kinases are responsible for phosphorylation tau, but which of these is responsible for this task is still unclear and requires further research [58]. Also, previous studies have shown that both oral intake and injection (i.p.) of GT can lead to the regulation of the protein tau, suppress the sarkosyl-soluble phosphorylated isoform, and have a positive effect on behavioral tasks [54].