NLRP3-dependent microglial training impaired the clearance of amyloid-beta and aggravated the cognitive decline in Alzheimer’s disease

He, Xiaofei; Xu, Jiadai; Li, Ge; Li, Mingyue; Li, Lili; Pei, Zhong; Zhang, Liying; Hu, Xiquan

doi:10.1038/s41419-020-03072-x

Cited by 46 publications

(35 citation statements)

References 36 publications

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“…The COVID-19 patients have a higher level of NLRP3 inflammasome activation that in combination with interleukin-18 and interleukin-1β have been shown to adversely impact cerebral function [ 22 ]. Also, NLRP3 inflammasome-mediated systemic inflammation can lead to pathological accumulation of the peptides/proteins such as fibrillar amyloid-β resulting in the induction and aggravation of neurodegenerative illnesses such as Alzheimer's disease [ 146 , 147 ]. It has been suggested that SARS-COV-2 infection may impair cognitive function that would lead to brain fog via selective targeting of the mitochondria of the neurons [ 104 ].…”

Section: Discussionmentioning

confidence: 99%

Long COVID, a comprehensive systematic scoping review

et al. 2021

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Purpose To find out what is known from literature about Long COVID until January 30, 2021. Methods We undertook a four-step search with no language restriction. A preliminary search was made to identify the keywords. A search strategy of all electronic databases resulted in 66 eligible studies. A forward and backward search of the references and citations resulted in additional 54 publications. Non-English language articles were translated using Google Translate. We conducted our scoping review based on the PRISMA-ScR Checklist. Results Of 120 papers, we found only one randomized clinical trial. Of the 67 original studies, 22 were cohort, and 28 were cross-sectional studies. Of the total 120 publications, 49.1% focused on signs and symptoms, 23.3% on management, and 10.8% on pathophysiology. Ten publications focused on imaging studies. The results are also presented extensively in a narrative synthesis in separated sections (nomenclature, diagnosis, pathophysiology, risk factors, signs/symptoms, management). Conclusions The controversies in its definition have impaired proper recognition and management. The predominant symptoms were: fatigue, breathlessness, arthralgia, sleep difficulties, and chest pain. Recent reports also point to the risk of long-term sequela with cutaneous, respiratory, cardiovascular, musculoskeletal, mental health, neurologic, and renal involvement in those who survive the acute phase of the illness. Supplementary Information The online version contains supplementary material available at 10.1007/s15010-021-01666-x.

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Section: Discussionmentioning

confidence: 99%

Long COVID, a comprehensive systematic scoping review

et al. 2021

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“…The COVID-19 patients have a higher level of NLRP3 inflammasome activation that in combination with interleukin-18 and interleukin-1β have been shown to adversely impact cerebral function (22). Also, NLRP3 inflammasome mediated systemic inflammation can lead to pathological accumulation of the peptides/proteins such as fibrillar amyloid-β resulting in the induction and aggravation of neurodegenerative illnesses such as Alzheimer's disease (150,151). It has been suggested that SARS-COV-2 infection may impair cognitive function that would lead to brain fog via selective targeting of the mitochondria of the neurons (96).…”

Section: ) Pathophysiologymentioning

confidence: 99%

<strong>Long COVID, A Comprehensive Systematic Scoping Review</strong>

Akbarialiabad¹,

Taghrir²,

Abdollahi³

et al. 2021

Preprint

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Introduction: Despite more than one year passed since the first cases of SARS-CoV-2 were reported, there is still no consensus on the definition and clinical management of post-acute-COVID-19. The condition has heterogeneously been named as Chronic COVID syndrome, Post COVID-19 Syndrome, post-acute sequela of SARS-CoV-2 (PASC), and the more familiar long COVID. Method: In order to capture all relevant published studies, we undertook a multi-step search with no language restriction. The following four-step search strategy was utilized: First, a preliminary (limited) search was conducted on January 20, 2021, in Google Scholar and PubMed to identify the appropriate keywords. Then, on January 30, 2021, we adopted a search strategy of electronic databases from Cochrane Library, PsycINFO, PubMed, Embase, Scopus, and Web of sciences, using those keywords. Then, after duplicate removal, we screened all titles, abstracts, and full texts. This resulted in 66 eligible studies. Subsequently, after a forward and backward search of their references and citations an additional 54 publications were found, resulting in a total of 120 publications that formed the basis of the present analysis. The titles, abstracts, and full-texts of non-English articles were translated using Google Translate for further evaluation. We conducted our scoping review based on the PRISMA-ScR Checklist.Results: We found only one randomized clinical trial in our search. Of the 67 original studies, 22 were cohort and 28 were cross-sectional studies totaling 74.6% of the original studies. Of the total of 120 publications, 59 (49.1%) focused on signs and symptoms, 28 (23.3%) were focused on management, and 13 (10.8%) focused on pathophysiology. Ten (9%) publications focused on imaging studies. Ninety-one percent of the original investigations came from high and upper-middle-income countries, highlighting the scarcity of reports originating from low-income and lower-middle-income countries.Conclusion: The predominant symptoms among those with the so-called “Long COVID” were: fatigue, breathlessness, arthralgia, sleep difficulties, and chest pain. Recent reports also point to the risk of long-term sequela with cutaneous, respiratory, cardiovascular, musculoskeletal, mental health, neurologic, and renal involvement in those who survive the acute phase of the illness. The ambiguity and controversies in its definition have impaired proper recognition and management of those requiring additional support following the resolution of the acute phase of this infection. This has resulted in long-standing distress for the patients and their families. Our findings highlight the need for a multidisciplinary approach, support, and rehabilitation for these patients in terms of long-term mental and physical health.

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“…In a mouse model of sporadic Alzheimer’s disease (SAD) induced by streptozotocin (STZ) injection, the levels of NLRP3 in the cortex and hippocampus were increased in the STZ group compared with those in the sham group (He et al 2020 ). The symptoms of SAD, such as neuronal dysfunction, neuronal loss, and amyloid-β deposition, were aggravated by LPS treatment in an NLRP3-dependent manner, and genetic deletion of NLRP3 or an NLRP3 inhibitor, MCC950, prevented SAD symptoms via inhibition of NLRP3 inflammasome activation (He et al 2020 ).…”

Section: Nlrp3 Inflammasome-associated Diseasesmentioning

confidence: 99%

Therapeutic regulation of the NLRP3 inflammasome in chronic inflammatory diseases

et al. 2021

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Inflammasomes are cytosolic pattern recognition receptors that recognize pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) derived from invading pathogens and damaged tissues, respectively. Upon activation, the inflammasome forms a complex containing a receptor protein, an adaptor, and an effector to induce the autocleavage and activation of procaspase-1 ultimately culminating in the maturation and secretion of IL-1β and IL-18 and pyroptosis. Inflammasome activation plays an important role in host immune responses to pathogen infections and tissue repair in response to cellular damage. The NLRP3 inflammasome is a well-characterized pattern recognition receptor and is well known for its critical role in the regulation of immunity and the development and progression of various inflammatory diseases. In this review, we summarize recent efforts to develop therapeutic applications targeting the NLRP3 inflammasome to cure and prevent chronic inflammatory diseases. This review extensively discusses NLRP3 inflammasome-related diseases and current development of small molecule inhibitors providing beneficial information on the design of therapeutic strategies for NLRP3 inflammasome-related diseases. Additionally, small molecule inhibitors are classified depending on direct or indirect targeting mechanism to describe the current status of the development of pharmacological inhibitors.

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NLRP3-dependent microglial training impaired the clearance of amyloid-beta and aggravated the cognitive decline in Alzheimer’s disease

Cited by 46 publications

References 36 publications

Long COVID, a comprehensive systematic scoping review

Long COVID, a comprehensive systematic scoping review

<strong>Long COVID, A Comprehensive Systematic Scoping Review</strong>

Therapeutic regulation of the NLRP3 inflammasome in chronic inflammatory diseases

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