Resolution of neuroinflammation: mechanisms and potential therapeutic option

Dokalis, Nikolaos; Prinz, Marco

doi:10.1007/s00281-019-00764-1

Cited by 79 publications

(73 citation statements)

References 113 publications

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“…Although current research indicates a “disease driving” role for neuroinflammation in α‐synucleinopathies, it is not a stretch to design or test therapeutics to block the induction or halt further inflammation‐led destruction in the CNS. Based on this idea, one focus of current research is maintaining the balance between neuroinflammation and neurorepair and/or tissue healing in neurodegenerative disease models 88,89 . Indeed, there is evidence in animal models of PD 90 for an imbalance between disease driving neuroinflammation and proresolving processes, indicating targeting key proresolving lipid mediators known as resolvins may be beneficial for inflammation resolution 90‐92 .…”

Section: Inflammation In α‐Synucleinopathies: Challenges For Immunothmentioning

confidence: 99%

Inflammation in Experimental Models of α‐Synucleinopathies

et al. 2020

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Neuroinflammation has long been associated with central nervous system pathology in α‐synucleinopathy disorders including Parkinson's disease and multiple system atrophy. In the past decade, research‐focused efforts in preclinical and experimental models have rallied around this idea, and considerable effort has been made to delineate critical neuroinflammatory processes. In this article, we discuss challenges in preclinical research, notably the use of animal models to recapitulate and dissect disease phenotypes as well as the need for more sensitive, reliable radiotracers to detect on‐target efficacy of immunomodulatory treatments in both human Parkinson's disease as well as preclinical models. © 2020 International Parkinson and Movement Disorder Society

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Section: Inflammation In α‐Synucleinopathies: Challenges For Immunothmentioning

confidence: 99%

Inflammation in Experimental Models of α‐Synucleinopathies

et al. 2020

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“…Acute neuroinflammation is a key response to clear pathogens and to repair tissue damage. However, if acute neuroinflammation remains unresolved, it can lead to chronic inflammation and neurodegeneration [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

The Beneficial Roles of SIRT1 in Neuroinflammation-Related Diseases

Jiao

Gong

2020

Oxidative Medicine and Cellular Longevity

197

106

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Sirtuins are the class III of histone deacetylases whose deacetylate of histones is dependent on nicotinamide adenine dinucleotide (NAD+). Among seven sirtuins, SIRT1 plays a critical role in modulating a wide range of physiological processes, including apoptosis, DNA repair, inflammatory response, metabolism, cancer, and stress. Neuroinflammation is associated with many neurological diseases, including ischemic stroke, bacterial infections, traumatic brain injury, Alzheimer’s disease (AD), and Parkinson’s disease (PD). Recently, numerous studies indicate the protective effects of SIRT1 in neuroinflammation-related diseases. Here, we review the latest progress regarding the anti-inflammatory and neuroprotective effects of SIRT1. First, we introduce the structure, catalytic mechanism, and functions of SIRT1. Next, we discuss the molecular mechanisms of SIRT1 in the regulation of neuroinflammation. Finally, we analyze the mechanisms and effects of SIRT1 in several common neuroinflammation-associated diseases, such as cerebral ischemia, traumatic brain injury, spinal cord injury, AD, and PD. Taken together, this information implies that SIRT1 may serve as a promising therapeutic target for the treatment of neuroinflammation-associated disorders.

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“…Sterile inflammation initially leads to tissue damages [3] . Likewise, in ischemic stroke, brain inflammation causes neural cell death and has been considered to be an attractive target for reducing brain damages not only in experimental rodent models but also in human patients [4][5][6] . As inflammation occurs within a few days after stroke onset, innate immunity, in which microglia, macrophages, neutrophils, and γδT cells play major role, has been thought to account for neuroinflammation after stroke, where such inflammation disappears after 1 week of stroke onset [ Figure 1].…”

Section: Introductionmentioning

confidence: 99%

Resolution of inflammation and repair after ischemic brain injury

Yoshimura¹,

Ito²

2020

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After ischemic stroke, proinflammatory molecules known as danger-associated molecular patterns (DAMPs) originating from damaged brain cells recruit and activate immune cells (neutrophils, macrophages, lymphocytes) further eliciting innate and adaptive immunity. During the acute phase from day 1 to day 3 of the stroke onset, macrophages play a major role in the progression of inflammation, promoting the destruction of brain tissue. During the recovery phase, from day 3~4 to day 7 after stroke onset, infiltrating macrophages switch to repairing macrophages, which clear the DAMPs and promote tissue repair by producing neurotrophic factors. Adaptive immunity during the late or chronic phase (> day 7) of stroke has not been well investigated. Recent studies have also indicated that antigen-specific T cells, especially regulatory T cells (Tregs), play major roles in neural repair. This review focuses mainly on the resolution of inflammation and tissue repair by macrophages and Tregs.

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Resolution of neuroinflammation: mechanisms and potential therapeutic option

Cited by 79 publications

References 113 publications

Inflammation in Experimental Models of α‐Synucleinopathies

Inflammation in Experimental Models of α‐Synucleinopathies

The Beneficial Roles of SIRT1 in Neuroinflammation-Related Diseases

Resolution of inflammation and repair after ischemic brain injury

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