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Risk and Causality by Genetics, Gender, and Age
Published in Susmita Chowdhuri, M Safwan Badr, James A Rowley, Control of Breathing during Sleep, 2022
Moshe Y Prero, Nardine Zakhary, Sally Ibrahim, Kingman P Strohl
The evidence for OSA being a strong driver comes primarily from studies of interventions, when both are established and causality is implied by an interventional therapy that is directed primarily at the OSA. There are several reviews on these issues and chapters that address the literature. For our purposes, however, one knows that the incidence and prevalence of stroke rise with age, and obstructive sleep apnea, after adjustments, is a moderate and established independent risk factor for stroke (80). However, trials of CPAP for stroke prevention in sleep apnea patients have been largely disappointing. A second chronic disease of aging, dementia, involves a widespread synaptic loss in the neocortex and the hippocampus. Risk factors for dementia including hypertension, hypoperfusion, endothelial dysfunction, inflammation, and oxidative stress, are present in OSA patients. The hippocampus is negatively impacted in both OSA and Alzheimer's disease. OSA promotes hippocampal atrophy, which is associated with memory impairment (81). While there is a recent report that this process is improved by CPAP therapy, there is insufficient evidence that OSA treatment is an effective prevention strategy to reduce risk for cognitive decline in middle-aged persons and the elderly. The complexity of interactions, however, after a chronic disease like stroke or dementia is present, and the limitations of current OSA therapy are such that new paradigms will be needed, and even then in the end bidirectional interactions may be established at a sub-clinical level.
Chronic Fatigue Syndrome: Limbic Encephalopathy in a Dysregulated Neuroimmune Network
Published in Jay A. Goldstein, Chronic Fatigue Syndromes, 2020
The most convincing clinical experience suggesting a central cause for fatigue is that of George Karpati, a neuropathologist at the Montreal Neurological Institute, where Wilder Penfield did his pioneering neurosurgical work. Dr. Karpati reports on stereotactic brain stimulation in patients with intractable epilepsy being considered for ablative surgery. Some of the patients, when being stimulated in the medial temporal lobe, report a sudden onset of severe fatigue, “like someone turned on a faucet and drained all the energy out of me.” 3 Although electrode stimulation of the brain is an imprecise technique, this finding is what one would expect. The amygdala and hippocampus are located in the medial temporal lobe, as is the dentate gyms adjacent to the hippocampus. The granule cells of the dentate gyms have the highest concentration of IL-1 receptors in the brain, and if cytokines are involved in causing fatigue, as one would expect from the fatiguing malaise associated with infections and therapeutic administration of alpha interferon and interleukin-2, the medial temporal lobe is where a fatigue center should be.
Basic Learning Processes and Eating Behavior
Published in Emily Crews Splane, Neil E. Rowland, Anaya Mitra, Psychology of Eating, 2019
Emily Crews Splane, Neil E. Rowland, Anaya Mitra
The neurobiology associated with conditioned taste aversions and preferences is different from that associated with innately disliked and liked tastes (which were mentioned in earlier chapters). The brain regions associated with learned taste dislikes and likes include those associated with memory, emotion, and reward (see Figure 7.2). It seems obvious that emotional memory (e.g., disgust) is important in preventing an organism from re-exposing itself to a dangerous food or flavor, as the lack of this recall ability could result in fatality. And, pleasant experiences with particular foods, such as warm soup on a chilly night or a substantive pasta dish following an exhausting soccer game, should be remembered so that those positive experiences can be repeated. These types of emotional memories require an intact hippocampus. Severe damage to the hippocampus disrupts the ability to form new explicit memories (i.e., memories that can be consciously recalled). Amnesic patients with hippocampal damage will consume a second meal soon after eating a first meal, and often a third meal as well, indicating that physiological satiety signals are not sufficient in regulating their food intake (Rozin et al., 1998). It seems, rather, that memory for food intake (type and amount of food) is more important in making subsequent food choices (Benoit, Davis & Davidson, 2010).
Decline of stress resilience in aging rats: Focus on choroid plexus-cerebrospinal fluid-hippocampus
Published in The World Journal of Biological Psychiatry, 2023
Kaige Liu, Huizhen Li, Ningxi Zeng, Wenjun Lu, Xiaofeng Wu, Hanfang Xu, Can Yan, Lili Wu
Hippocampus is intimately linked to emotion and cognition, and susceptible to brain injury from ageing and stress (Corr et al. 2022). Some investigators believed changes in stress response were associated with hippocampal volume, which decreased in stress-resilient animals (Tse et al. 2014). The rodent hippocampus generating new neurons throughout life is called hippocampal neurogenesis, which is one of the forms of neural plasticity (Moreno-Jiménez et al. 2021). Adult hippocampal neurogenesis alterations are emerging as an important method for predicting behaviour changes, namely resilience or susceptibility (Jones et al. 2022). Animals exposed to various stress protocols were shown to have reduced adult hippocampal neurogenesis. Predictable stress, on the other hand, increases adult hippocampal neurogenesis and leads to stress resilience. Most studies show that neurogenesis-ablated animals do not exhibit a depressive phenotype, but when stressed, they exhibit enhanced responsiveness and stress susceptibility, suggesting that adult hippocampal neurogenesis is important in the stress response and may be linked to stress resilience (Levone et al. 2015). In this study, ACUMS rats exhibited exacerbated hippocampal neurogenesis dysfunction and apoptosis compared to CUMS rats, which might be one of the pathological bases of resilience decline.
Laterality in functional and metabolic state of the bulbectomised rat brain detected by ASL and 1H MRS: A pilot study
Published in The World Journal of Biological Psychiatry, 2023
Iveta Pavlova, Eva Drazanova, Lucie Kratka, Petra Amchova, Ondrej Macicek, Jana Starcukova, Zenon Starcuk, Jana Ruda-Kucerova
Hippocampus is the brain structure responsible for memory formation, spatial memory and navigation, and the transfer of long-term memories (Guy-Evans 2021). In addition, it is related to the olfactory response as the memory of odours (Guy-Evans 2021); thus, differences in the metabolic state of the hippocampus in the OBX model were expected. In the right hippocampus of the OBX rats, we found significantly lower Cho/NAA and Cho/tCr levels than in the SHAM. Still, no difference in the left hippocampus was found, confirming Ende et al. (2000) MDD clinical study result and Hong et al. (2009) preclinical forced swimming test study outcome, but reportedly in the opposite hemisphere. We assume that this result may reflect the role of choline in acetylcholine production and release, thus a lower ability of memory storage in OBX rats (Harkin et al. 2003; Song and Leonard 2005); which is in agreement with the MDD studies reporting memory deficit (Xi et al. 2011).
Is tDCS a potential first line treatment for major depression?
Published in International Review of Psychiatry, 2021
Rachel Woodham, Rachael M. Rimmer, Julian Mutz, Cynthia H. Y. Fu
Widespread functional and structural abnormalities are observed in major depression (Wise et al., 2017). In particular, bilateral reductions in hippocampal volume are one of the most common findings (Cole et al., 2011; Schmaal et al., 2016). Located within the limbic system in the medial temporal lobe, the hippocampus plays a central role in learning and memory. It is a plastic brain structure, in which excitatory amino acids neurotransmitters and NMDA receptors are involved in the damaging effects of stress and trauma on function and structure (McEwen, 1999). Neuroplastic changes in the hippocampus are associated with changes in mood, and hippocampal grey matter volume is state dependent (Arnone et al., 2013). Clinical efficacy of antidepressant medication is proposed to be mediated through neural plasticity (Castrén & Hen, 2013; Fu et al., 2020; Santarelli et al., 2003; Warner-Schmidt & Duman, 2006). Treatment with antidepressant drugs can stimulate neurogenesis in the hippocampus and restore grey matter to a volume similar to that in both healthy participants and patients in remission (Arnone et al., 2013; Warner-Schmidt & Duman, 2006). At the cellular level, animal models show increased postsynaptic spine density and enhanced synaptic plasticity following treatment with fluoxetine (Ampuero et al., 2010). Increases in BDNF serum levels, indicating increased neuroplasticity, are observed following treatment with antidepressant medication which are associated with improvements in depressive symptoms (Brunoni et al., 2008; Duman & Monteggia, 2006).