Neuroinflammation, the thread connecting neurological disease

Brambilla, Roberta

doi:10.1007/s00401-019-02009-9

Cited by 37 publications

(19 citation statements)

References 9 publications

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“…Moreover, once activated, aged microglia are more resistant to regulation (Norden and Godbout, 2013), which can be a contributing factor to the progression of neurodegenerative diseases, as active microglia synthesize and release neurotoxic substances that cause further neuronal damage (Lull and Block, 2010). In a healthy environment, activation of microglia serves as a protective mechanism, however, due to the complex and multifactorial nature of microglial activation, subtle changes may lead to amplified or dysfunctional activation which is thought to enhance neurodegenerative pathology, with cytokines presenting at almost all disease phases (Brambilla, 2019).…”

Section: Neuronal Signals That Affect Neuroinflammationmentioning

confidence: 99%

Neuromodulation of Glial Function During Neurodegeneration

Stevenson

Samokhina

Rossetti

et al. 2020

Front. Cell. Neurosci.

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Glia, a non-excitable cell type once considered merely as the connective tissue between neurons, is nowadays acknowledged for its essential contribution to multiple physiological processes including learning, memory formation, excitability, synaptic plasticity, ion homeostasis, and energy metabolism. Moreover, as glia are key players in the brain immune system and provide structural and nutritional support for neurons, they are intimately involved in multiple neurological disorders. Recent advances have demonstrated that glial cells, specifically microglia and astroglia, are involved in several neurodegenerative diseases including Amyotrophic lateral sclerosis (ALS), Epilepsy, Parkinson's disease (PD), Alzheimer's disease (AD), and frontotemporal dementia (FTD). While there is compelling evidence for glial modulation of synaptic formation and regulation that affect neuronal signal processing and activity, in this manuscript we will review recent findings on neuronal activity that affect glial function, specifically during neurodegenerative disorders. We will discuss the nature of each glial malfunction, its specificity to each disorder, overall contribution to the disease progression and assess its potential as a future therapeutic target.

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Section: Neuronal Signals That Affect Neuroinflammationmentioning

confidence: 99%

Neuromodulation of Glial Function During Neurodegeneration

Stevenson

Samokhina

Rossetti

et al. 2020

Front. Cell. Neurosci.

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“…One common feature of most cytokines is their pleiotropic nature. The same cytokine can trigger an inflammatory cascade that can have detrimental or protective functions in disease progression depending on timing, area of action, or cellular source (Becher et al, 2017;Brambilla, 2019). For example, tumor necrosis factor (TNF) is one of the most widely studied cytokines in stroke, and preclinical data indicates both neurotoxic and neuroprotective effects of TNF.…”

Section: Introductionmentioning

confidence: 99%

Neuroinflammation Treatment via Targeted Delivery of Nanoparticles

Cerqueira

Ayad

Lee

2020

Front. Cell. Neurosci.

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The lack of effective treatments for most neurological diseases has prompted the search for novel therapeutic options. Interestingly, neuroinflammation is emerging as a common feature to target in most CNS pathologies. Recent studies suggest that targeted delivery of small molecules to reduce neuroinflammation can be beneficial. However, suboptimal drug delivery to the CNS is a major barrier to modulate inflammation because neurotherapeutic compounds are currently being delivered systemically without spatial or temporal control. Emerging nanomaterial technologies are providing promising and superior tools to effectively access neuropathological tissue in a controlled manner. Here we highlight recent advances in nanomaterial technologies for drug delivery to the CNS. We propose that state-of-the-art nanoparticle drug delivery platforms can significantly impact local CNS bioavailability of pharmacological compounds and treat neurological diseases.

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“…The increasing awareness of the involvement of the immune system, not only in the progression but also directly related to the onset of CNS diseases, has fueled a renewed interest in the field in recent years [12][13][14]. Indeed, neuroinflammation has been linked to Parkinson's disease (PD) [15], Alzheimer's disease (AD) [16,17], amyotrophic lateral sclerosis (ALS) [18] and other CNS disorders, such as multiple sclerosis [19], traumatic brain injury [20], depression [21] and schizophrenia [22], among others.…”

Section: Introductionmentioning

confidence: 99%

“…The involvement of the neuroinflammatory landscape in such diseases reinforces the notion that overstimulation of the immune response is a major determinant in the pathophysiology of these diseases. Three main factors appear to be key across all the cited diseases, which in many respects are complementary in nature: (i) cytokines, whether in a damaging or protective capacity (or both), are involved in the different disease stages, holding pleiotropic and systemic effects and displaying variations in number and phenotypic features in all cell types; (ii) glial cell activation is an early and persistent feature in the course of the disease, whose phenotype and function may change over time; (iii) a whole constellation of neuron-glia interactions sustain and propagate the neuroinflammatory response [13]. While current treatments for most CNS pathologies arguably have limited efficacy, IL-1R1 represents a worthwhile target in the search for neuroinflammation-associated CNS diseases therapeutics, due to its central role in the immune response.…”

Section: Introductionmentioning

confidence: 99%

The Therapeutic Prospects of Targeting IL-1R1 for the Modulation of Neuroinflammation in Central Nervous System Disorders

Luís

Simões

Brito

2022

IJMS

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The interleukin-1 receptor type 1 (IL-1R1) holds pivotal roles in the immune system, as it is positioned at the “epicenter” of the inflammatory signaling networks. Increased levels of the cytokine IL-1 are a recognized feature of the immune response in the central nervous system (CNS) during injury and disease, i.e., neuroinflammation. Despite IL-1/IL-1R1 signaling within the CNS having been the subject of several studies, the roles of IL-1R1 in the CNS cellular milieu still cause controversy. Without much doubt, however, the persistent activation of the IL-1/IL-1R1 signaling pathway is intimately linked with the pathogenesis of a plethora of CNS disease states, ranging from Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS), all the way to schizophrenia and prion diseases. Importantly, a growing body of evidence is showing that blocking IL-1R1 signaling via pharmacological or genetic means in different experimental models of said CNS diseases leads to reduced neuroinflammation and delayed disease progression. The aim of this paper is to review the recent progress in the study of the biological roles of IL-1R1, as well as to highlight key aspects that render IL-1R1 a promising target for the development of novel disease-modifying treatments for multiple CNS indications.

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Neuroinflammation, the thread connecting neurological disease

Cited by 37 publications

References 9 publications

Neuromodulation of Glial Function During Neurodegeneration

Neuromodulation of Glial Function During Neurodegeneration

Neuroinflammation Treatment via Targeted Delivery of Nanoparticles

The Therapeutic Prospects of Targeting IL-1R1 for the Modulation of Neuroinflammation in Central Nervous System Disorders

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