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      Peripheral inflammation and neurocognitive impairment: correlations, underlying mechanisms, and therapeutic implications

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          Abstract

          Cognitive impairments, such as learning and memory deficits, may occur in susceptible populations including the elderly and patients who are chronically ill or have experienced stressful events, including surgery, infection, and trauma. Accumulating lines of evidence suggested that peripheral inflammation featured by the recruitment of peripheral immune cells and the release of pro-inflammatory cytokines may be activated during aging and these conditions, participating in peripheral immune system-brain communication. Lots of progress has been achieved in deciphering the core bridging mechanism connecting peripheral inflammation and cognitive impairments, which may be helpful in developing early diagnosis, prognosis evaluation, and prevention methods based on peripheral blood circulation system sampling and intervention. In this review, we summarized the evolving evidence on the prevalence of peripheral inflammation-associated neurocognitive impairments and discussed the research advances in the underlying mechanisms. We also highlighted the prevention and treatment strategies against peripheral inflammation-associated cognitive dysfunction.

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          Most cited references189

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          Hallmarks of aging: An expanding universe

          Aging is driven by hallmarks fulfilling the following three premises: (1) their age-associated manifestation, (2) the acceleration of aging by experimentally accentuating them, and (3) the opportunity to decelerate, stop, or reverse aging by therapeutic interventions on them. We propose the following twelve hallmarks of aging: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. These hallmarks are interconnected among each other, as well as to the recently proposed hallmarks of health, which include organizational features of spatial compartmentalization, maintenance of homeostasis, and adequate responses to stress.
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            Normal gut microbiota modulates brain development and behavior

            Microbial colonization of mammals is an evolution-driven process that modulate host physiology, many of which are associated with immunity and nutrient intake. Here, we report that colonization by gut microbiota impacts mammalian brain development and subsequent adult behavior. Using measures of motor activity and anxiety-like behavior, we demonstrate that germ free (GF) mice display increased motor activity and reduced anxiety, compared with specific pathogen free (SPF) mice with a normal gut microbiota. This behavioral phenotype is associated with altered expression of genes known to be involved in second messenger pathways and synaptic long-term potentiation in brain regions implicated in motor control and anxiety-like behavior. GF mice exposed to gut microbiota early in life display similar characteristics as SPF mice, including reduced expression of PSD-95 and synaptophysin in the striatum. Hence, our results suggest that the microbial colonization process initiates signaling mechanisms that affect neuronal circuits involved in motor control and anxiety behavior.
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              Mild respiratory COVID can cause multi-lineage neural cell and myelin dysregulation

              COVID survivors frequently experience lingering neurological symptoms that resemble cancer therapy-related cognitive impairment, a syndrome for which white-matter microglial reactivity and consequent neural dysregulation is central. Here, we explored the neurobiological effects of respiratory SARS-CoV-2 infection and found white-matter-selective microglial reactivity in mice and humans. Following mild respiratory COVID in mice, persistently impaired hippocampal neurogenesis, decreased oligodendrocytes and myelin loss were evident together with elevated CSF cytokines/chemokines including CCL11. Systemic CCL11 administration specifically caused hippocampal microglial reactivity and impaired neurogenesis. Concordantly, humans with lasting cognitive symptoms post-COVID exhibit elevated CCL11 levels. Compared to SARS-CoV-2, mild respiratory influenza in mice caused similar patterns of white matter-selective microglial reactivity, oligodendrocyte loss, impaired neurogenesis and elevated CCL11 at early timepoints, but after influenza only elevated CCL11 and hippocampal pathology persisted. These findings illustrate similar neuropathophysiology after cancer therapy and respiratory SARS-CoV-2 infection which may contribute to cognitive impairment following even mild COVID.
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                Author and article information

                Contributors
                URI : https://loop.frontiersin.org/people/1596714/overviewRole: Role: Role: Role: Role: Role: Role:
                URI : https://loop.frontiersin.org/people/1704934/overviewRole: Role: Role: Role:
                Role: Role: Role: Role: Role:
                URI : https://loop.frontiersin.org/people/1697722/overviewRole: Role: Role: Role: Role: Role: Role:
                URI : https://loop.frontiersin.org/people/1670312/overviewRole: Role: Role: Role: Role: Role: Role:
                Journal
                Front Aging Neurosci
                Front Aging Neurosci
                Front. Aging Neurosci.
                Frontiers in Aging Neuroscience
                Frontiers Media S.A.
                1663-4365
                29 November 2023
                2023
                : 15
                : 1305790
                Affiliations
                [1] 1Department of Anesthesiology, The First Affiliated Hospital of Guangxi Medical University , Nanning, China
                [2] 2Department of Anesthesiology, Hunan Provincial People’s Hospital, The First Affiliated Hospital of Hunan Normal University , Changsha, China
                [3] 3Guangxi Key Laboratory of Enhanced Recovery after Surgery for Gastrointestinal Cancer, The First Affiliated Hospital of Guangxi Medical University , Nanning, China
                Author notes

                Edited by: Chengjin Gao, Shanghai Jiao Tong University, China

                Reviewed by: Shaowei Jiang, Jiahui International Hospital, China; Jie Zhang, Huazhong University of Science and Technology, China

                *Correspondence: Lai Wei, 448027999@ 123456qq.com
                Article
                10.3389/fnagi.2023.1305790
                10716308
                38094503
                d4eed833-c594-4a7a-b1ae-1f2e2b6bb1e7
                Copyright © 2023 Tan, Chen, Kong, Wei and Xie.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 02 October 2023
                : 10 November 2023
                Page count
                Figures: 5, Tables: 0, Equations: 0, References: 189, Pages: 19, Words: 17902
                Funding
                The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants partly from the Special Fund of Neurotoxicity of General Anesthetics and its Prevention and Treatment Innovation Team of the First Affiliated Hospital of Guangxi Medical University (No. YYZS2022001), the Guangxi Clinical Research Center for Anesthesiology (No. GK AD22035214), and the Department of Science and Technology of Hunan Province (No. 2021SK50907).
                Categories
                Aging Neuroscience
                Review
                Custom metadata
                Neuroinflammation and Neuropathy

                Neurosciences
                peripheral inflammation,neurocognitive impairment,large-scale brain functional network,fmri,neuroinflammation

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