Journal articles: 'Chronic neuroinflammation'

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Vergne-Salle, Pascale, and Philippe Bertin. "Chronic pain and neuroinflammation." Joint Bone Spine 88, no. 6 (December 2021): 105222. http://dx.doi.org/10.1016/j.jbspin.2021.105222.

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Chen, Shih-Heng, Shuangyu Han, Chih-Fen Hu, Ran Zhou, Yun Gao, Dezhen Tu, Huiming Gao, et al. "Activation of the MAC1-ERK1/2-NOX2 Pathway Is Required for LPS-Induced Sustaining Reactive Microgliosis, Chronic Neuroinflammation and Neurodegeneration." Antioxidants 11, no. 6 (June 20, 2022): 1202. http://dx.doi.org/10.3390/antiox11061202.

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Recent studies suggest that improper resolution of acute neuroinflammation may lead to long-lasting low-grade chronic neuroinflammation and drive progressive neurodegeneration. However, the molecular mechanism underlying the transition from acute to chronic neuroinflammation remains unclear. The main purpose of this study was to search for potential pathways mediating LPS-elicited chronic neuroinflammation and resultant neurodegeneration. Using microglia cultures prepared from C57BL/6J, MAC1-deficient, and MyD88-deficient mice, the initial study showed that activation of TLR-4 is not sufficient for maintaining chronic neuroinflammation despite its essential role in LPS-initiated acute neuroinflammation. Opposite to TLR-4, our studies showed significantly reduced intensity of chronic neuroinflammation, oxidative stress, and progressive loss of nigral dopaminergic neurons in MAC1-deficient neuron/glial cultures or mice stimulated with LPS. Mechanistic studies revealed the essential role ERK1/2 activation in chronic neuroinflammation-elicited neurodegeneration, which was demonstrated by using an ERK1/2 inhibitor in neuron-glial cultures. Taken together, we propose a key role of the MAC1-NOX2-ERK1/2 signaling pathway in the initiation and maintenance of low-grade chronic neuroinflammation. Continuing ERK1/2 phosphorylation and NOX2 activation form a vicious feedforward cycle in microglia to maintain the low-grade neuroinflammation and drive neurodegeneration.

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Aloisi, Francesca, Sandra Columba-Cabezas, Diego Franciotta, Barbara Rosicarelli, Roberta Magliozzi, Richard Reynolds, Elena Ambrosini, Eliana Coccia, Marco Salvetti, and Barbara Serafini. "Lymphoid chemokines in chronic neuroinflammation." Journal of Neuroimmunology 198, no. 1-2 (July 2008): 106–12. http://dx.doi.org/10.1016/j.jneuroim.2008.04.025.

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Ji, Ru-Rong, Andrea Nackley, Yul Huh, Niccolò Terrando, and William Maixner. "Neuroinflammation and Central Sensitization in Chronic and Widespread Pain." Anesthesiology 129, no. 2 (August 1, 2018): 343–66. http://dx.doi.org/10.1097/aln.0000000000002130.

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Abstract Chronic pain is maintained in part by central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is also driven by neuroinflammation in the peripheral and central nervous system. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines. Recent studies suggest that central cytokines and chemokines are powerful neuromodulators and play a sufficient role in inducing hyperalgesia and allodynia after central nervous system administration. Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites. Thus, neuroinflammation drives widespread chronic pain via central sensitization. We also discuss sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain.

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Driessen, Alexandria K., Anna-Claire Devlin, Fionnuala T. Lundy, S. Lorraine Martin, Gerard P. Sergeant, Stuart B. Mazzone, and Lorcan P. McGarvey. "Perspectives on neuroinflammation contributing to chronic cough." European Respiratory Journal 56, no. 4 (July 9, 2020): 2000758. http://dx.doi.org/10.1183/13993003.00758-2020.

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Chronic cough can be a troublesome clinical problem. Current thinking is that increased activity and/or enhanced sensitivity of the peripheral and central neural pathways mediates chronic cough via processes similar to those associated with the development of chronic pain. While inflammation is widely thought to be involved in the development of chronic cough, the true mechanisms causing altered neural activity and sensitisation remain largely unknown. In this back-to-basics perspective article we explore evidence that inflammation in chronic cough may, at least in part, involve neuroinflammation orchestrated by glial cells of the nervous system. We summarise the extensive evidence for the role of both peripheral and central glial cells in chronic pain, and hypothesise that the commonalities between pain and cough pathogenesis and clinical presentation warrant investigations into the neuroinflammatory mechanisms that contribute to chronic cough. We open the debate that glial cells may represent an underappreciated therapeutic target for controlling troublesome cough in disease.

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Persidsky, Yuri, Jeremy Hill, Ming Zhang, Holly Dykstra, Malika Winfield, Nancy L. Reichenbach, Raghava Potula, Abir Mukherjee, Servio H. Ramirez, and Slava Rom. "Dysfunction of brain pericytes in chronic neuroinflammation." Journal of Cerebral Blood Flow & Metabolism 36, no. 4 (September 30, 2015): 794–807. http://dx.doi.org/10.1177/0271678x15606149.

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Brain pericytes are uniquely positioned within the neurovascular unit to provide support to blood brain barrier (BBB) maintenance. Neurologic conditions, such as HIV-1-associated neurocognitive disorder, are associated with BBB compromise due to chronic inflammation. Little is known about pericyte dysfunction during HIV-1 infection. We found decreased expression of pericyte markers in human brains from HIV-1-infected patients (even those on antiretroviral therapy). Using primary human brain pericytes, we assessed expression of pericyte markers (α1-integrin, α-smooth muscle actin, platelet-derived growth factor-B receptor β, CX-43) and found their downregulation after treatment with tumor necrosis factor-α (TNFα) or interleukin-1 β (IL-1β). Pericyte exposure to virus or cytokines resulted in decreased secretion of factors promoting BBB formation (angiopoietin-1, transforming growth factor-β1) and mRNA for basement membrane components. TNFα and IL-1β enhanced expression of adhesion molecules in pericytes paralleling increased monocyte adhesion to pericytes. Monocyte migration across BBB models composed of human brain endothelial cells and pericytes demonstrated a diminished rate in baseline migration compared to constructs composed only of brain endothelial cells. However, exposure to the relevant chemokine, CCL2, enhanced the magnitude of monocyte migration when compared to BBB models composed of brain endothelial cells only. These data suggest an important role of pericytes in BBB regulation in neuroinflammation.

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Ji, Ru-Rong, Zhen-Zhong Xu, and Yong-Jing Gao. "Emerging targets in neuroinflammation-driven chronic pain." Nature Reviews Drug Discovery 13, no. 7 (June 20, 2014): 533–48. http://dx.doi.org/10.1038/nrd4334.

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Delery, Elizabeth C., and Andrew G. MacLean. "Chronic Viral Neuroinflammation: Speculation on Underlying Mechanisms." Viral Immunology 32, no. 1 (February 2019): 55–62. http://dx.doi.org/10.1089/vim.2018.0093.

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Kirk, S. L., and S. J. Karlik. "VEGF and vascular changes in chronic neuroinflammation." Journal of Autoimmunity 21, no. 4 (December 2003): 353–63. http://dx.doi.org/10.1016/s0896-8411(03)00139-2.

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Mawey, Feytie Magda, Azimatul Karimah, Erlyn Limoa, and Muhammad Nazmuddin. "Neuroinflammation in Schizophrenia." Jurnal Psikiatri Surabaya 10, no. 1 (May 31, 2021): 1. http://dx.doi.org/10.20473/jps.v10i1.20871.

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Schizophrenia is a chronic debilitating mental illness. In many aspects, the neuropathology of schizophrenia is closely associated with neuroinflammation, especially microglial activation. Microglial hyperactivity, which is characterized by the predominant release of proinflammatory cytokines serves as the basis of the neuroinflammation hypothesis in schizophrenia. The enhanced inflammatory induce neuronal susceptibility to oxidative stress and trigger, glutamatergic synaptic dysregulation, especially in the mesolimbic and mesocortical pathways. Many in vitro studies, in vivo animal evidence, post-mortem examinations, neuroimaging evaluations with Positron Emission Tomography (PET), anti-inflammatory and antipsychotic use converge upon the central role of microglial activation and proinflammatory cytokines as common of features schizophrenia.

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Shastri, Abhishek, Domenico Marco Bonifati, and Uday Kishore. "Innate Immunity and Neuroinflammation." Mediators of Inflammation 2013 (2013): 1–19. http://dx.doi.org/10.1155/2013/342931.

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Inflammation of central nervous system (CNS) is usually associated with trauma and infection. Neuroinflammation occurs in close relation to trauma, infection, and neurodegenerative diseases. Low-level neuroinflammation is considered to have beneficial effects whereas chronic neuroinflammation can be harmful. Innate immune system consisting of pattern-recognition receptors, macrophages, and complement system plays a key role in CNS homeostasis following injury and infection. Here, we discuss how innate immune components can also contribute to neuroinflammation and neurodegeneration.

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Nivrenjeet, Singh, Siti Waheeda Mohd-Zin, Singh Nisheljeet, Abu Bakar Azizi, Kamalanathan Palaniandy, Mohd Firdaus-Raih, Mohd Hisam Muhamad Ariffin, Nicholas Daniel Edward Greene, and Noraishah Mydin Abdul-Aziz. "Inflammation in embryology: A review of neuroinflammation in spina bifida." Neuroscience Research Notes 5, no. 1 (April 1, 2022): 132. http://dx.doi.org/10.31117/neuroscirn.v5i1.132.

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The occurrence of neuroinflammation after the failure of neural tube closure, resulting in spina bifida aperta, is well established but whether or not neuroinflammation contributes to damage to the neuroepithelium prior to and during closure is not known. Neuroinflammation may occur at different time periods after perturbation to the developing spinal cord. Evidence suggests that early neuroinflammation is detrimental, whereas the later chronic phase of neuroinflammation may have useful roles. The role of neuroinflammation in neural tube defects is complex. It is important to make the distinction of whether neuroinflammation is important for neuroprotection or detrimental to the neural tissue. This may directly be influenced by the location, magnitude and duration of the insult, as well as the expression of neurotrophic or neurotoxic molecules. The current understanding remains that the chronic damage to the developing spinal cord is likely due to the chemical and mechanical damage of the exposed neural tissue owing to the aggressive intrauterine environment, described as the “two-hit mechanism”. Astrogliosis in the exposed spinal cord has been described in animal models of spina bifida after the failure of closure during embryonic life. Still, its association with neuroinflammatory processes is poorly understood. In this review, we will discuss the current understanding of neuroinflammation in neural tube defects, specifically spina bifida, and highlight inflammation-targeted strategies that may potentially be used to treat this pathophysiological condition.

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Tran, Shirley, Sanjaya Kuruppu, and Niwanthi W. Rajapakse. "Chronic Renin-Angiotensin System Activation Induced Neuroinflammation: Common Mechanisms Underlying Hypertension and Dementia?" Journal of Alzheimer's Disease 85, no. 3 (February 1, 2022): 943–55. http://dx.doi.org/10.3233/jad-215231.

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Hypertension is a major risk factor for the pathogenesis of vascular dementia and Alzheimer’s disease. Chronic activation of the renin-angiotensin system (RAS) contributes substantially to neuroinflammation. We propose that neuroinflammation arising from chronic RAS activation can initiate and potentiate the onset of hypertension and related dementia. Neuroinflammation induced by chronic activation of the RAS plays a key role in the pathogenesis of dementia. Increased levels of pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and transforming growth factor (TGF)-β have been reported in brain tissue of vascular dementia patients and animal models of vascular dementia induced by either angiotensin II infusion or transverse aortic coarctation. It is proposed that neuronal cell death and synaptic dysfunction induced by neuroinflammation lead to cognitive impairment in dementia. The neuroprotective RAS pathway, regulated by angiotensin-converting enzyme 2 (ACE2) which converts angiotensin II into angiotensin-(1–7), can attenuate hypertension and dementia. Furthermore, the use of anti-hypertensive medications in preventing dementia or cognitive decline in hypertensive patients and animal models of dementia have mostly been beneficial. Current evidence suggests a strong link between RAS induced neuroinflammation and the onset of hypertension and dementia, which warrants further investigation. Strategies to counteract an overactive RAS and enhance the neuroprotective arm of the RAS may help prevent or improve cognitive impairment associated with hypertension.

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Matsushita, Kazutoshi, Masayuki Taniguchi, and Tomoyuki Furuyashiki. "Left-right asymmetry in chronic stress-induced neuroinflammation." Proceedings for Annual Meeting of The Japanese Pharmacological Society 94 (2021): 3—P1–18. http://dx.doi.org/10.1254/jpssuppl.94.0_3-p1-18.

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Felipo, Vicente, Carmina Montoliu, and Marta Llansola. "Neuroinflammation and neurological alterations in chronic liver diseases." Neuroimmunology and Neuroinflammation 2, no. 3 (2015): 138. http://dx.doi.org/10.4103/2347-8659.160845.

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Paterka, Magdalena, Valerie Staudt, Eva Reuter, Frauke Zipp, and Tobias Bopp. "The role of NFATc2 in chronic autoimmune neuroinflammation." Journal of Neuroimmunology 275, no. 1-2 (October 2014): 168. http://dx.doi.org/10.1016/j.jneuroim.2014.08.451.

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Qin, Liya, Xuefei Wu, Michelle L. Block, Yuxin Liu, George R. Breese, Jau-Shyong Hong, Darin J. Knapp, and Fulton T. Crews. "Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration." Glia 55, no. 5 (2007): 453–62. http://dx.doi.org/10.1002/glia.20467.

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Bossù, Paola, Elisa Toppi, Valentina Sterbini, and Gianfranco Spalletta. "Implication of Aging Related Chronic Neuroinflammation on COVID-19 Pandemic." Journal of Personalized Medicine 10, no. 3 (August 26, 2020): 102. http://dx.doi.org/10.3390/jpm10030102.

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SARS-CoV-2, the virus responsible for the COVID-19 pandemic, leads to a respiratory syndrome and other manifestations. Most affected people show no or mild symptoms, but the risk of severe disease and death increases in older people. Here, we report a narrative review on selected studies targeting aging-related chronic neuroinflammation in the COVID-19 pandemic. A hyperactivation of the innate immune system with elevated levels of pro-inflammatory cytokines occurs during severe COVID-19, pointing to an important role of the innate immune dysregulation in the disease outcome. Aging is characterized by a general condition of low-grade inflammation, also connected to chronic inflammation of the brain (neuroinflammation), which is involved in frailty syndrome and contributes to several age-associated diseases, including neurodegenerative and neuropsychiatric disorders. Since neuroinflammation can be induced or worsened by the virus infection itself, as well as by stressful conditions like those linked to the recent pandemic, the role of neuroinflammatory mechanisms could be central in a vicious circle leading to an increase in the mortality risk in aged COVID-19 patients. Furthermore, triggered neuroinflammatory pathways and consequent neurodegenerative and neuropsychiatric conditions might be potential long-term complications of COVID-19. In order to provide insights to help clinicians in identifying patients who progress to a more severe case of the disease, this review underlines the potential implications of aging-related neuroinflammation in COVID-19 pandemic.

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Gao, Yun, Dezhen Tu, Ru Yang, Chun-Hsien Chu, Jau-Shyong Hong, and Hui-Ming Gao. "Through Reducing ROS Production, IL-10 Suppresses Caspase-1-Dependent IL-1β Maturation, thereby Preventing Chronic Neuroinflammation and Neurodegeneration." International Journal of Molecular Sciences 21, no. 2 (January 11, 2020): 465. http://dx.doi.org/10.3390/ijms21020465.

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Chronic neuroinflammation contributes to the pathogenesis of Parkinson’s disease (PD). However, cellular and molecular mechanisms by which chronic neuroinflammation is formed and maintained remain elusive. This study aimed to explore detailed mechanisms by which anti-inflammatory cytokine interleukin-10 (IL-10) prevented chronic neuroinflammation and neurodegeneration. At 24 h after an intranigral injection of lipopolysaccharide (LPS), levels of NLRP3, pro-caspase-1, pro-IL-1β, active caspase-1, and mature IL-1β in the midbrain were much higher in IL-10−/− mice than wildtype mice. Mechanistically, IL-10−/− microglia produced more intracellular reactive oxygen species (iROS) and showed more profound activation of NADPH oxidase (NOX2) than wildtype microglia. Meanwhile, suppression of NOX2-derived iROS production blocked LPS-elicited caspase-1 activation and IL-1β maturation in IL-10−/− microglia in vitro and in vivo. One month after intranigral LPS injection, IL-10−/− mice revealed more profound microglial activation and dopaminergic neurodegeneration in the substantia nigra than wildtype mice. Importantly, such PD-like pathological changes were prevented by IL-1β neutralization. Collectively, IL-10 inhibited LPS-elicited production of NOX2-derived iROS thereby suppressing synthesis of NLRP3, pro-caspase-1 and pro-IL-1β and their activation and cleavage. By this mechanism, IL-10 prevented chronic neuroinflammation and neurodegeneration. This study suggested boosting anti-inflammatory effects of IL-10 and suppressing NLRP3 inflammasome activation could be beneficial for PD treatment.

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Hasriadi, Peththa Wadu Dasuni Wasana, Opa Vajragupta, Pornchai Rojsitthisak, and Pasarapa Towiwat. "Mechanistic Insight into the Effects of Curcumin on Neuroinflammation-Driven Chronic Pain." Pharmaceuticals 14, no. 8 (August 7, 2021): 777. http://dx.doi.org/10.3390/ph14080777.

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Chronic pain is a persistent and unremitting condition that has immense effects on patients’ quality of life. Studies have shown that neuroinflammation is associated with the induction and progression of chronic pain. The activation of microglia and astrocytes is the major hallmark of spinal neuroinflammation leading to neuronal excitability in the projection neurons. Excessive activation of microglia and astrocytes is one of the major contributing factors to the exacerbation of pain. However, the current chronic pain treatments, mainly by targeting the neuronal cells, remain ineffective and unable to meet the patients’ needs. Curcumin, a natural plant product found in the Curcuma genus, improves chronic pain by diminishing the release of inflammatory mediators from the spinal glia. This review details the role of curcumin in microglia and astrocytes both in vitro and in vivo and how it improves pain. We also describe the mechanism of curcumin by highlighting the major glia-mediated cascades in pain. Moreover, the role of curcumin on inflammasome and epigenetic regulation is discussed. Furthermore, we discuss the strategies used to improve the efficacy of curcumin. This review illustrates that curcumin modulating microglia and astrocytes could assure the treatment of chronic pain by suppressing spinal neuroinflammation.

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Tian, Zhengming, Xunming Ji, and Jia Liu. "Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects." International Journal of Molecular Sciences 23, no. 11 (June 2, 2022): 6224. http://dx.doi.org/10.3390/ijms23116224.

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Vascular cognitive impairment and dementia (VCID) is a major heterogeneous brain disease caused by multiple factors, and it is the second most common type of dementia in the world. It is caused by long-term chronic low perfusion in the whole brain or local brain area, and it eventually develops into severe cognitive dysfunction syndrome. Because of the disease’s ambiguous classification and diagnostic criteria, there is no clear treatment strategy for VCID, and the association between cerebrovascular pathology and cognitive impairment is controversial. Neuroinflammation is an immunological cascade reaction mediated by glial cells in the central nervous system where innate immunity resides. Inflammatory reactions could be triggered by various damaging events, including hypoxia, ischemia, and infection. Long-term chronic hypoperfusion-induced ischemia and hypoxia can overactivate neuroinflammation, causing apoptosis, blood–brain barrier damage and other pathological changes, triggering or aggravating the occurrence and development of VCID. In this review, we will explore the mechanisms of neuroinflammation induced by ischemia and hypoxia caused by chronic hypoperfusion and emphasize the important role of neuroinflammation in the development of VCID from the perspective of immune cells, immune mediators and immune signaling pathways, so as to provide valuable ideas for the prevention and treatment of the disease.

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Andronie-Cioara, Felicia Liana, Adriana Ioana Ardelean, Carmen Delia Nistor-Cseppento, Anamaria Jurcau, Maria Carolina Jurcau, Nicoleta Pascalau, and Florin Marcu. "Molecular Mechanisms of Neuroinflammation in Aging and Alzheimer’s Disease Progression." International Journal of Molecular Sciences 24, no. 3 (January 18, 2023): 1869. http://dx.doi.org/10.3390/ijms24031869.

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Aging is the most prominent risk factor for late-onset Alzheimer’s disease. Aging associates with a chronic inflammatory state both in the periphery and in the central nervous system, the evidence thereof and the mechanisms leading to chronic neuroinflammation being discussed. Nonetheless, neuroinflammation is significantly enhanced by the accumulation of amyloid beta and accelerates the progression of Alzheimer’s disease through various pathways discussed in the present review. Decades of clinical trials targeting the 2 abnormal proteins in Alzheimer’s disease, amyloid beta and tau, led to many failures. As such, targeting neuroinflammation via different strategies could prove a valuable therapeutic strategy, although much research is still needed to identify the appropriate time window. Active research focusing on identifying early biomarkers could help translating these novel strategies from bench to bedside.

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I, Hassanin. "Care Giving As a Chronic Psychosocial Distress: Neuroinflammation Trajectory." Egyptian Journal of Geriatrics and Gerontology 3, no. 1 (March 1, 2016): 1–10. http://dx.doi.org/10.21608/ejgg.2016.30865.

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Giraldo-Velásquez, Manuel F., Nicolas I. Pérez-Osorio, Alejandro Espinosa-Cerón, Brandon M. Bárcena, Arturo Calderón-Gallegos, Gladis Fragoso, Mónica Torres-Ramos, Nayeli Páez-Martínez, and Edda Sciutto. "Intranasal Methylprednisolone Ameliorates Neuroinflammation Induced by Chronic Toluene Exposure." Pharmaceutics 14, no. 6 (June 2, 2022): 1195. http://dx.doi.org/10.3390/pharmaceutics14061195.

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Inhalants are chemical substances that induce intoxication, and toluene is the main component of them. Increasing evidence indicates that a dependence on inhalants involves a state of chronic stress associated to the activation of immune cells in the central nervous system and release of proinflammatory mediators, especially in some brain areas such as the nucleus accumbens and frontal cortex, where the circuits of pleasure and reward are. In this study, anti-neuroinflammatory treatment based on a single dose of intranasal methylprednisolone was assessed in a murine model of chronic toluene exposure. The levels of proinflammatory mediators, expression levels of Iba-1 and GFAP, and histological changes in the frontal cortex and nucleus accumbens were evaluated after the treatment. The chronic exposure to toluene significantly increased the levels of TNF-α, IL-6, and NO, the expression of GFAP, and induced histological alterations in mouse brains. The treatment with intranasally administered MP significantly reduced the expression of TNF-α and NO and the expression of GFAP (p < 0.05); additionally, it reversed the central histological damage. These results indicate that intranasally administered methylprednisolone could be considered as a treatment to reverse neuroinflammation and histological damages associated with the use of inhalants.

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Hein, Amy M., and M. Kerry O’Banion. "Neuroinflammation and Cognitive Dysfunction in Chronic Disease and Aging." Journal of Neuroimmune Pharmacology 7, no. 1 (January 18, 2012): 3–6. http://dx.doi.org/10.1007/s11481-011-9340-1.

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Tang, Chuan-Feng, Cong-Ying Wang, Jun-Han Wang, Qiao-Na Wang, Shen-Jie Li, Hai-Ou Wang, Feng Zhou, and Jian-Mei Li. "Short-Chain Fatty Acids Ameliorate Depressive-Like Behaviors of High Fructose-Fed Mice by Rescuing Hippocampal Neurogenesis Decline and Blood–Brain Barrier Damage." Nutrients 14, no. 9 (April 29, 2022): 1882. http://dx.doi.org/10.3390/nu14091882.

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Excessive fructose intake is associated with the increased risk of mental illness, such as depression, but the underlying mechanisms are poorly understood. Our previous study found that high fructose diet (FruD)-fed mice exhibited neuroinflammation, hippocampal neurogenesis decline and blood–brain barrier (BBB) damage, accompanied by the reduction of gut microbiome-derived short-chain fatty acids (SCFAs). Here, we found that chronic stress aggravated these pathological changes and promoted the development of depressive-like behaviors in FruD mice. In detail, the decreased number of newborn neurons, mature neurons and neural stem cells (NSCs) in the hippocampus of FruD mice was worsened by chronic stress. Furthermore, chronic stress exacerbated the damage of BBB integrity with the decreased expression of zonula occludens-1 (ZO-1), claudin-5 and occludin in brain vasculature, overactivated microglia and increased neuroinflammation in FruD mice. These results suggest that high fructose intake combined with chronic stress leads to cumulative negative effects that promote the development of depressive-like behaviors in mice. Of note, SCFAs could rescue hippocampal neurogenesis decline, improve BBB damage and suppress microglia activation and neuroinflammation, thereby ameliorate depressive-like behaviors of FruD mice exposed to chronic stress. These results could be used to develop dietary interventions to prevent depression.

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Ribarič, Samo. "Physical Exercise, a Potential Non-Pharmacological Intervention for Attenuating Neuroinflammation and Cognitive Decline in Alzheimer’s Disease Patients." International Journal of Molecular Sciences 23, no. 6 (March 17, 2022): 3245. http://dx.doi.org/10.3390/ijms23063245.

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This narrative review summarises the evidence for considering physical exercise (PE) as a non-pharmacological intervention for delaying cognitive decline in patients with Alzheimer’s disease (AD) not only by improving cardiovascular fitness but also by attenuating neuroinflammation. Ageing is the most important risk factor for AD. A hallmark of the ageing process is a systemic low-grade chronic inflammation that also contributes to neuroinflammation. Neuroinflammation is associated with AD, Parkinson’s disease, late-onset epilepsy, amyotrophic lateral sclerosis and anxiety disorders. Pharmacological treatment of AD is currently limited to mitigating the symptoms and attenuating progression of the disease. AD animal model studies and human studies on patients with a clinical diagnosis of different stages of AD have concluded that PE attenuates cognitive decline not only by improving cardiovascular fitness but possibly also by attenuating neuroinflammation. Therefore, low-grade chronic inflammation and neuroinflammation should be considered potential modifiable risk factors for AD that can be attenuated by PE. This opens the possibility for personalised attenuation of neuroinflammation that could also have important health benefits for patients with other inflammation associated brain disorders (i.e., Parkinson’s disease, late-onset epilepsy, amyotrophic lateral sclerosis and anxiety disorders). In summary, life-long, regular, structured PE should be considered as a supplemental intervention for attenuating the progression of AD in human. Further studies in human are necessary to develop optimal, personalised protocols, adapted to the progression of AD and the individual’s mental and physical limitations, to take full advantage of the beneficial effects of PE that include improved cardiovascular fitness, attenuated systemic inflammation and neuroinflammation, stimulated brain Aβ peptides brain catabolism and brain clearance.

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Bok, Eugene, Myungjin Jo, Shinrye Lee, Bo-Ram Lee, Jaekwang Kim, and Hyung-Jun Kim. "Dietary Restriction and Neuroinflammation: A Potential Mechanistic Link." International Journal of Molecular Sciences 20, no. 3 (January 22, 2019): 464. http://dx.doi.org/10.3390/ijms20030464.

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Chronic neuroinflammation is a common feature of the aged brain, and its association with the major neurodegenerative changes involved in cognitive impairment and motor dysfunction is well established. One of the most potent antiaging interventions tested so far is dietary restriction (DR), which extends the lifespan in various organisms. Microglia and astrocytes are two major types of glial cells involved in the regulation of neuroinflammation. Accumulating evidence suggests that the age-related proinflammatory activation of astrocytes and microglia is attenuated under DR. However, the molecular mechanisms underlying DR-mediated regulation of neuroinflammation are not well understood. Here, we review the current understanding of the effects of DR on neuroinflammation and suggest an underlying mechanistic link between DR and neuroinflammation that may provide novel insights into the role of DR in aging and age-associated brain disorders.

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Bynoe, Margaret S. "NAFLD induces neuroinflammation and accelerates Alzheimer’s disease." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 188.4. http://dx.doi.org/10.4049/jimmunol.196.supp.188.4.

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Abstract Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease afflicting about one third of the world’s population and 30% of the US population. It is induced by consumption of high lipid diets and is characterized by liver inflammation and subsequent liver pathology leading to steatosis and steatohepatitis. We fed mice with high fat/lipid diet (HFD) or a standard diet (SD) and monitored them for signs of systemic or central nervous system inflammation. We found that NAFLD induced acute liver inflammation and accelerates signs of Alzheimer’s disease (AD) in an AD-Transgenic model. Moreover, chronic NAFLD induced advanced signs of AD in WT mice. In the chronic disease stage, we observed neuronal apoptosis and decreased brain expression of low-density lipoprotein receptor-related protein-1 that is involved in beta-amyloid clearance, in both WT and APP-Tg mice. HFD fed mice harbored numerous activated and proliferating microglial cells in their brain. Removal of mice from HFD during acute disease reversed liver pathology and neuroinflammation and decreased beta-amyloid plaque load. Concomitant with microglial cell activation, we observed profound changes in microbiota, resulting in a more pathogenic microglial phenotype. Interestingly, removal of mice from HFD completely abrogated microglial cell activation and proliferation and changes in gut. Based on these findings, we conclude that inflammation induced by HFD induces profound pathogenic changes in the gut concomitant with pathogenic changes in the CNS leading to neurodegeneration.

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Chen, Szu-Han, Chia-Ching Wu, Sheng-Che Lin, Wan-Ling Tseng, Tzu-Chieh Huang, Anjali Yadav, Fu-I. Lu, Ya-Hsin Liu, Shau-Ping Lin, and Yuan-Yu Hsueh. "Investigation of Neuropathology after Nerve Release in Chronic Constriction Injury of Rat Sciatic Nerve." International Journal of Molecular Sciences 22, no. 9 (April 29, 2021): 4746. http://dx.doi.org/10.3390/ijms22094746.

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Peripheral compressive neuropathy causes significant neuropathic pain, muscle weakness and prolong neuroinflammation. Surgical decompression remains the gold standard of treatment but the outcome is suboptimal with a high recurrence rate. From mechanical compression to chemical propagation of the local inflammatory signals, little is known about the distinct neuropathologic patterns and the genetic signatures after nerve decompression. In this study, controllable mechanical constriction forces over rat sciatic nerve induces irreversible sensorimotor dysfunction with sustained local neuroinflammation, even 4 weeks after nerve release. Significant gene upregulations are found in the dorsal root ganglia, regarding inflammatory, proapoptotic and neuropathic pain signals. Genetic profiling of neuroinflammation at the local injured nerve reveals persistent upregulation of multiple genes involving oxysterol metabolism, neuronal apoptosis, and proliferation after nerve release. Further validation of the independent roles of each signal pathway will contribute to molecular therapies for compressive neuropathy in the future.

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SCHOENBERG, Poppy L. A., and Katlyn M. Gonzalez. "Allostatic Mechanism of Mind-Body Medicine for Neuroinflammation." OBM Integrative and Complementary Medicine 08, no. 01 (January 12, 2023): 1–15. http://dx.doi.org/10.21926/obm.icm.2301005.

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Chronic inflammatory diseases are the most significant cause of death in the world and entail severe impairment to quality of life. The World Health Organization (WHO) ranks chronic inflammatory diseases as the greatest threat to human health and wellbeing. Inflammation is epicentral to many clinical conditions and symptoms, and it is anticipated that the health, economic, and mortality burdens associated with chronic inflammation will steadily increase in the United States over the next 30 years. An inflammatory model of disease premises that peripheral injury/trauma/toxins release signaling mediators that activate glial components of peripheral and central cellular circuitry which if prolonged causes toxification of the central nervous system, or neuroinflammation. This inflammatory process is associated with an array of systemic symptomatology affecting somatic, neurocognitive, and affective domains, that can often be misdiagnosed and/or ineffectively treated in the clinic. Centralized neuroinflammation determines a range of conditions and their clinical trajectories, from autoimmune diseases, cancers, cardiovascular diseases, chronic pain, to neurological and psychiatric disorders. It is coming to light that mind-body medicine, defined here as mindfulness- and yoga-based interventions, appear to modulate peripheral cell signaling involved with inflammatory response. Translational mechanism nor intervention specificity of this early data is currently clearly delineated, posing an exciting and highly beneficial frontier for further empirical exploration in the field of integrative mind-body medicine. Here we initiate an allostasis model of working mechanism that aims to inform methodological design and ensuing empirical perspectives.

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Steve Michael Blake, Panida Piboolnurak, Patricia Lynn Borman, Thomas Harding, and Catherine Peterson Blake. "Reducing neuroinflammation in Parkinson’s disease with dietary compounds." GSC Biological and Pharmaceutical Sciences 18, no. 2 (February 28, 2022): 026–37. http://dx.doi.org/10.30574/gscbps.2022.18.2.0052.

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Emerging evidence indicates that chronic brain inflammation may lead to oxidation and death of dopaminergic neurons in Parkinson’s disease (PD). Increased levels of pro-inflammatory cytokines have been found in brain and cerebrospinal fluid in PD patients. Higher inflammation is associated with poorer motor function and cognition in PD. Data from postmortem studies show the increased presence of activated microglial cells expressing inflammatory cytokines in the substantia nigra of PD patients. When aberrant proteins, such as alpha-synuclein, activate microglia, a self-sustaining cycle of neuroinflammation may kill off dopaminergic brain cells. Reducing brain inflammation may slow down neuronal death and disease progression, especially if instituted early in disease progression. We will review dietary triggers of inflammation and ways to ameliorate chronic inflammation. We will introduce four key dietary compounds that can be avoided to decrease inflammation and oxidation: Arachidonic acid, lipopolysaccharides, dairy products, and advanced glycation endproducts. We will also review many dietary compounds that can reduce chronic inflammation and oxidation, potentially reducing the risk and progression of PD.

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Santoni, Angela, Matteo Santoni, and Edoardo Arcuri. "Chronic Cancer Pain: Opioids within Tumor Microenvironment Affect Neuroinflammation, Tumor and Pain Evolution." Cancers 14, no. 9 (April 30, 2022): 2253. http://dx.doi.org/10.3390/cancers14092253.

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Pain can be a devastating experience for cancer patients, resulting in decreased quality of life. In the last two decades, immunological and pain research have demonstrated that pain persistence is primarily caused by neuroinflammation leading to central sensitization with brain neuroplastic alterations and changes in pain responsiveness (hyperalgesia, and pain behavior). Cancer pain is markedly affected by the tumor microenvironment (TME), a complex ecosystem consisting of different cell types (cancer cells, endothelial and stromal cells, leukocytes, fibroblasts and neurons) that release soluble mediators triggering neuroinflammation. The TME cellular components express opioid receptors (i.e., MOR) that upon engagement by endogenous or exogenous opioids such as morphine, initiate signaling events leading to neuroinflammation. MOR engagement does not only affect pain features and quality, but also influences directly and/or indirectly tumor growth and metastasis. The opioid effects on chronic cancer pain are also clinically characterized by altered opioid responsiveness (tolerance and hyperalgesia), a hallmark of the problematic long-term treatment of non-cancer pain. The significant progress made in understanding the immune-mediated development of chronic pain suggests its exploitation for novel alternative immunotherapeutic approaches.

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Onyango, Isaac G., Gretsen V. Jauregui, Mária Čarná, James P. Bennett, and Gorazd B. Stokin. "Neuroinflammation in Alzheimer’s Disease." Biomedicines 9, no. 5 (May 7, 2021): 524. http://dx.doi.org/10.3390/biomedicines9050524.

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Alzheimer’s disease (AD) is a neurodegenerative disease associated with human aging. Ten percent of individuals over 65 years have AD and its prevalence continues to rise with increasing age. There are currently no effective disease modifying treatments for AD, resulting in increasingly large socioeconomic and personal costs. Increasing age is associated with an increase in low-grade chronic inflammation (inflammaging) that may contribute to the neurodegenerative process in AD. Although the exact mechanisms remain unclear, aberrant elevation of reactive oxygen and nitrogen species (RONS) levels from several endogenous and exogenous processes in the brain may not only affect cell signaling, but also trigger cellular senescence, inflammation, and pyroptosis. Moreover, a compromised immune privilege of the brain that allows the infiltration of peripheral immune cells and infectious agents may play a role. Additionally, meta-inflammation as well as gut microbiota dysbiosis may drive the neuroinflammatory process. Considering that inflammatory/immune pathways are dysregulated in parallel with cognitive dysfunction in AD, elucidating the relationship between the central nervous system and the immune system may facilitate the development of a safe and effective therapy for AD. We discuss some current ideas on processes in inflammaging that appear to drive the neurodegenerative process in AD and summarize details on a few immunomodulatory strategies being developed to selectively target the detrimental aspects of neuroinflammation without affecting defense mechanisms against pathogens and tissue damage.

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Puhakka, Noora, Shalini Das Gupta, Niina Vuokila, and Asla Pitkänen. "Transfer RNA-Derived Fragments and isomiRs Are Novel Components of Chronic TBI-Induced Neuropathology." Biomedicines 10, no. 1 (January 8, 2022): 136. http://dx.doi.org/10.3390/biomedicines10010136.

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Neuroinflammation is a secondary injury mechanism that evolves in the brain for months after traumatic brain injury (TBI). We hypothesized that an altered small non-coding RNA (sncRNA) signature plays a key role in modulating post-TBI secondary injury and neuroinflammation. At 3threemonths post-TBI, messenger RNA sequencing (seq) and small RNAseq were performed on samples from the ipsilateral thalamus and perilesional cortex of selected rats with a chronic inflammatory endophenotype, and sham-operated controls. The small RNAseq identified dysregulation of 2 and 19 miRNAs in the thalamus and cortex, respectively. The two candidates from the thalamus and the top ten from the cortex were selected for validation. In the thalamus, miR-146a-5p and miR-155-5p levels were upregulated, and in the cortex, miR-375-3p and miR-211-5p levels were upregulated. Analysis of isomiRs of differentially expressed miRNAs identified 3′ nucleotide additions that were increased after TBI. Surprisingly, we found fragments originating from 16 and 13 tRNAs in the thalamus and cortex, respectively. We further analyzed two upregulated fragments, 3′tRF-IleAAT and 3′tRF-LysTTT. Increased expression of the full miR-146a profile, and 3′tRF-IleAAT and 3′tRF-LysTTT was associated with a worse behavioral outcome in animals with chronic neuroinflammation. Our results highlight the importance of understanding the regulatory roles of as-yet unknown sncRNAs for developing better strategies to treat TBI and neuroinflammation.

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Li, Hojun, Leslie A. Benson, Lauren A. Henderson, Isaac H. Solomon, Alyssa L. Kennedy, Ariane Soldatos, Bibiana Bielekova, et al. "Central nervous system–restricted familial hemophagocytic lymphohistiocytosis responds to hematopoietic cell transplantation." Blood Advances 3, no. 4 (February 13, 2019): 503–7. http://dx.doi.org/10.1182/bloodadvances.2018027417.

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Marcos, José Luis, Rossy Olivares-Barraza, Karina Ceballo, Melisa Wastavino, Víctor Ortiz, Julio Riquelme, Jonathan Martínez-Pinto, Pablo Muñoz, Gonzalo Cruz, and Ramón Sotomayor-Zárate. "Obesogenic Diet-Induced Neuroinflammation: A Pathological Link between Hedonic and Homeostatic Control of Food Intake." International Journal of Molecular Sciences 24, no. 2 (January 11, 2023): 1468. http://dx.doi.org/10.3390/ijms24021468.

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Obesity-induced neuroinflammation is a chronic aseptic central nervous system inflammation that presents systemic characteristics associated with increased pro-inflammatory cytokines such as interleukin 1 beta (IL-1β) and interleukin 18 (IL-18) and the presence of microglia and reactive astrogliosis as well as the activation of the NLRP3 inflammasome. The obesity pandemic is associated with lifestyle changes, including an excessive intake of obesogenic foods and decreased physical activity. Brain areas such as the lateral hypothalamus (LH), lateral septum (LS), ventral tegmental area (VTA), and nucleus accumbens (NAcc) have been implicated in the homeostatic and hedonic control of feeding in experimental models of diet-induced obesity. In this context, a chronic lipid intake triggers neuroinflammation in several brain regions such as the hypothalamus, hippocampus, and amygdala. This review aims to present the background defining the significant impact of neuroinflammation and how this, when induced by an obesogenic diet, can affect feeding control, triggering metabolic and neurological alterations.

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Al-Nusaif, Murad, Yushan Lin, Tianbai Li, Cheng Cheng, and Weidong Le. "Advances in NURR1-Regulated Neuroinflammation Associated with Parkinson’s Disease." International Journal of Molecular Sciences 23, no. 24 (December 19, 2022): 16184. http://dx.doi.org/10.3390/ijms232416184.

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Neuroinflammation plays a crucial role in the progression of neurodegenerative disorders, particularly Parkinson’s disease (PD). Glial cell activation and subsequent adaptive immune involvement are neuroinflammatory features in familial and idiopathic PD, resulting in the death of dopaminergic neuron cells. An oxidative stress response, inflammatory mediator production, and immune cell recruitment and activation are all hallmarks of this activation, leading to chronic neuroinflammation and progressive neurodegeneration. Several studies in PD patients’ cerebrospinal fluid and peripheral blood revealed alterations in inflammatory markers and immune cell populations that may lead to or exacerbate neuroinflammation and perpetuate the neurodegenerative process. Most of the genes causing PD are also expressed in astrocytes and microglia, converting their neuroprotective role into a pathogenic one and contributing to disease onset and progression. Nuclear receptor-related transcription factor 1 (NURR1) regulates gene expression linked to dopaminergic neuron genesis and functional maintenance. In addition to playing a key role in developing and maintaining neurotransmitter phenotypes in dopaminergic neurons, NURR1 agonists have been shown to reverse behavioral and histological abnormalities in animal PD models. NURR1 protects dopaminergic neurons from inflammation-induced degeneration, specifically attenuating neuronal death by suppressing the expression of inflammatory genes in microglia and astrocytes. This narrative review highlights the inflammatory changes in PD and the advances in NURR1-regulated neuroinflammation associated with PD. Further, we present new evidence that targeting this inflammation with a variety of potential NURR1 target therapy medications can effectively slow the progression of chronic neuroinflammation-induced PD.

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Malaguarnera, Michele, Tiziano Balzano, Mari Carmen Castro, Marta Llansola, and Vicente Felipo. "The Dual Role of the GABAA Receptor in Peripheral Inflammation and Neuroinflammation: A Study in Hyperammonemic Rats." International Journal of Molecular Sciences 22, no. 13 (June 24, 2021): 6772. http://dx.doi.org/10.3390/ijms22136772.

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Cognitive and motor impairment in minimal hepatic encephalopathy (MHE) are mediated by neuroinflammation, which is induced by hyperammonemia and peripheral inflammation. GABAergic neurotransmission in the cerebellum is altered in rats with chronic hyperammonemia. The mechanisms by which hyperammonemia induces neuroinflammation remain unknown. We hypothesized that GABAA receptors can modulate cerebellar neuroinflammation. The GABAA antagonist bicuculline was administrated daily (i.p.) for four weeks in control and hyperammonemic rats. Its effects on peripheral inflammation and on neuroinflammation as well as glutamate and GABA neurotransmission in the cerebellum were assessed. In hyperammonemic rats, bicuculline decreases IL-6 and TNFα and increases IL-10 in the plasma, reduces astrocyte activation, induces the microglia M2 phenotype, and reduces IL-1β and TNFα in the cerebellum. However, in control rats, bicuculline increases IL-6 and decreases IL-10 plasma levels and induces microglial activation. Bicuculline restores the membrane expression of some glutamate and GABA transporters restoring the extracellular levels of GABA in hyperammonemic rats. Blocking GABAA receptors improves peripheral inflammation and cerebellar neuroinflammation, restoring neurotransmission in hyperammonemic rats, whereas it induces inflammation and neuroinflammation in controls. This suggests a complex interaction between GABAergic and immune systems. The modulation of GABAA receptors could be a suitable target for improving neuroinflammation in MHE.

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He, Jingyi, Guofu Zhu, Guoqing Wang, and Feng Zhang. "Oxidative Stress and Neuroinflammation Potentiate Each Other to Promote Progression of Dopamine Neurodegeneration." Oxidative Medicine and Cellular Longevity 2020 (July 3, 2020): 1–12. http://dx.doi.org/10.1155/2020/6137521.

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Parkinson’s disease (PD) is a chronic and complex disease of the central nervous system (CNS). Progressive loss of dopamine (DA) neurons in midbrain substantia nigra is considered to be the main cause of PD. The hallmark of PD pathology is the formation of Lewy bodies and the deposition of α-synuclein (α-syn). The mechanisms responsible for the progressive feature of DA neurodegeneration are not fully illustrated. Recently, oxidative stress and neuroinflammation have received extensive attention as two important entry points in the pathogenesis of PD. The occurrence of oxidative stress and neuroinflammation is usually derived from external influences or changes in internal environment, such as the accumulation of reactive oxygen species, exposure to a toxic environment, and the transformation of systemic inflammation. However, PD never results from a single independent factor and the simultaneous participation of oxidative stress and neuroinflammation contributed to PD development. Oxidative stress and neuroinflammation could potentiate each other to promote progression of PD. In this review, we briefly summarized the conditions of oxidative stress and neuroinflammation and the crosstalk between oxidative stress and neuroinflammation on the development of PD.

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Santiago, Ana R., Filipa I. Baptista, Paulo F. Santos, Gonçalo Cristóvão, António F. Ambrósio, Rodrigo A. Cunha, and Catarina A. Gomes. "Role of Microglia Adenosine A2AReceptors in Retinal and Brain Neurodegenerative Diseases." Mediators of Inflammation 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/465694.

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Neuroinflammation mediated by microglial cells in the brain has been commonly associated with neurodegenerative diseases. Whether this microglia-mediated neuroinflammation is cause or consequence of neurodegeneration is still a matter of controversy. However, it is unequivocal that chronic neuroinflammation plays a role in disease progression and halting that process represents a potential therapeutic strategy. The neuromodulator adenosine emerges as a promising targeting candidate based on its ability to regulate microglial proliferation, chemotaxis, and reactivity through the activation of its G protein coupledA2Areceptor (A2AR). This is in striking agreement with the ability ofA2ARblockade to control several brain diseases. Retinal degenerative diseases have been also associated with microglia-mediated neuroinflammation, but the role ofA2ARhas been scarcely explored. This review aims to compare inflammatory features of Parkinson’s and Alzheimer’s diseases with glaucoma and diabetic retinopathy, discussing the therapeutic potential ofA2ARin these degenerative conditions.

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Khadka, Bikram, Jae-Young Lee, Dong Ho Park, Ki-Taek Kim, and Jong-Sup Bae. "The Role of Natural Compounds and their Nanocarriers in the Treatment of CNS Inflammation." Biomolecules 10, no. 10 (October 1, 2020): 1401. http://dx.doi.org/10.3390/biom10101401.

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Neuroinflammation, which is involved in various inflammatory cascades in nervous tissues, can result in persistent and chronic apoptotic neuronal cell death and programmed cell death, triggering various degenerative disorders of the central nervous system (CNS). The neuroprotective effects of natural compounds against neuroinflammation are mainly mediated by their antioxidant, anti-inflammatory, and antiapoptotic properties that specifically promote or inhibit various molecular signal transduction pathways. However, natural compounds have several limitations, such as their pharmacokinetic properties and stability, which hinder their clinical development and use as medicines. This review discusses the molecular mechanisms of neuroinflammation and degenerative diseases of CNS. In addition, it emphasizes potential natural compounds and their promising nanocarriers for overcoming their limitations in the treatment of neuroinflammation. Moreover, recent promising CNS inflammation-targeted nanocarrier systems implementing lesion site-specific active targeting strategies for CNS inflammation are also discussed.

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Lainez, Nancy M., and Djurdjica Coss. "Obesity, Neuroinflammation, and Reproductive Function." Endocrinology 160, no. 11 (September 12, 2019): 2719–36. http://dx.doi.org/10.1210/en.2019-00487.

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Abstract The increasing occurrence of obesity has become a significant public health concern. Individuals with obesity have higher prevalence of heart disease, stroke, osteoarthritis, diabetes, and reproductive disorders. Reproductive problems include menstrual irregularities, pregnancy complications, and infertility due to anovulation, in women, and lower testosterone and diminished sperm count, in men. In particular, women with obesity have reduced levels of both gonadotropin hormones, and, in obese men, lower testosterone is accompanied by diminished LH. Taken together, these findings indicate central dysregulation of the hypothalamic–pituitary–gonadal axis, specifically at the level of the GnRH neuron function, which is the final brain output for the regulation of reproduction. Obesity is a state of hyperinsulinemia, hyperlipidemia, hyperleptinemia, and chronic inflammation. Herein, we review recent advances in our understanding of how these metabolic and immune changes affect hypothalamic function and regulation of GnRH neurons. In the latter part, we focus on neuroinflammation as a major consequence of obesity and discuss findings that reveal that GnRH neurons are uniquely positioned to respond to inflammatory changes.

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Bajwa, Ekta, Caitlin B. Pointer, and Andis Klegeris. "The Role of Mitochondrial Damage-Associated Molecular Patterns in Chronic Neuroinflammation." Mediators of Inflammation 2019 (April 1, 2019): 1–11. http://dx.doi.org/10.1155/2019/4050796.

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Mitochondrial dysfunction has been established as a common feature of neurodegenerative disorders that contributes to disease pathology by causing impaired cellular energy production. Mitochondrial molecules released into the extracellular space following neuronal damage or death may also play a role in these diseases by acting as signaling molecules called damage-associated molecular patterns (DAMPs). Mitochondrial DAMPs have been shown to initiate proinflammatory immune responses from nonneuronal glial cells, including microglia and astrocytes; thereby, they have the potential to contribute to the chronic neuroinflammation present in these disorders accelerating the degeneration of neurons. In this review, we highlight the mitochondrial DAMPs cytochrome c (CytC), mitochondrial transcription factor A (TFAM), and cardiolipin and explore their potential role in the central nervous system disorders including Alzheimer’s disease and Parkinson’s disease, which are characterized by neurodegeneration and chronic neuroinflammation.

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Ren, Jinxuan, Lina Yu, Jiaqi Lin, Longfei Ma, Dave Schwinn Gao, Na Sun, Ying Liu, et al. "Dimethyl itaconate inhibits neuroinflammation to alleviate chronic pain in mice." Neurochemistry International 154 (March 2022): 105296. http://dx.doi.org/10.1016/j.neuint.2022.105296.

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Omdal, Roald. "The biological basis of chronic fatigue: neuroinflammation and innate immunity." Current Opinion in Neurology 33, no. 3 (June 2020): 391–96. http://dx.doi.org/10.1097/wco.0000000000000817.

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Baker, L. M., B. Hauss-Wegrzyniak, and G. L. Wenk. "The effect of a novel NO-NSAID on chronic neuroinflammation." Journal of Neuroimmunology 90, no. 1 (September 1998): 79. http://dx.doi.org/10.1016/s0165-5728(98)91653-8.

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Hansson, Elisabeth. "Neuroinflammation and glial cell activation in pathogenesis of chronic pain." Scandinavian Journal of Pain 6, no. 1 (January 1, 2015): 1–2. http://dx.doi.org/10.1016/j.sjpain.2014.10.004.

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López-González, Irene, Raquel Pinacho, Èlia Vila, Ana Escanilla, Isidre Ferrer, and Belén Ramos. "Neuroinflammation in the dorsolateral prefrontal cortex in elderly chronic schizophrenia." European Neuropsychopharmacology 29, no. 3 (March 2019): 384–96. http://dx.doi.org/10.1016/j.euroneuro.2018.12.011.

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Faucard, Raphaël, Alexandra Madeira, Nadège Gehin, François-Jérôme Authier, Petrica-Adrian Panaite, Catherine Lesage, Ingrid Burgelin, et al. "Human Endogenous Retrovirus and Neuroinflammation in Chronic Inflammatory Demyelinating Polyradiculoneuropathy." EBioMedicine 6 (April 2016): 190–98. http://dx.doi.org/10.1016/j.ebiom.2016.03.001.

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Journal articles on the topic 'Chronic neuroinflammation'

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