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Does Parkinson Disease Affect The Immune System

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Does Parkinson Disease Affect The Immune System

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By Marta Pajares Marta Pajares Skillet Preprints.org Google Scholar 1, 2, Ana I. Rojo Ana I. Rojo Skillet Preprints.org Google Scholar 1, 2, 3, 4, Gina Menda Gina Menda Skillet Preprints.org Google Scholar 5, Lisardo Boscá Lisardo Boscá Scilit Preprints.org Google Scholar 1, 3, 6 and Antonius Cuadrado Antonius Cuadrado Scilit Preprints.org Google Scholar 1, 2, 3, 4, 5, *

Received: 17 June 2020 / Published: 11 July 2020 / Accepted: 13 July 2020 / Published: 14 July 2020

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Parkinson’s disease (PD) is a common neurodegenerative disorder, characterized primarily by the death of dopaminergic neurons that project from the substantia nigra. Although the molecular basis of the development of PD is still poorly defined, a large body of evidence from human and animal models supports the involvement of inflammation in its initiation or progression. However, the exact trigger for this response is unclear. Here we provide a systematic review of the cellular mediators, namely microglia, astroglia and endothelial cells. We also discuss the genetic and transcriptional control of inflammation in PD and the immunomodulatory role of dopamine and reactive oxygen species. Finally, we summarize preclinical and clinical approaches to PD neuroinflammation.

Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by impaired motor activities, mainly due to damage to the nigrostriatal dopaminergic system. Specifically, the death of dopaminergic neurons that project from the substantia nigra to the caudate-putamen in the striatum results in loss of dopamine neurotransmission, leading to early motor symptoms, including resting tremors, bradykinesia, rigidity, and postural instability. Although PD was initially characterized as a movement disorder without dementia, it is now accepted that the progression of PD affects other dopaminergic, cholinergic, and serotonergic pathways, leading to non-motor symptoms that also include anosmia, sleep disturbances, and constipation. such as cognitive and psychiatric symptoms. , such as dementia and depression [1, 2].

The onset of the disease is decades before the first symptoms appear; However, the ultimate cause of dopaminergic death remains unknown. While 5-10% of PD cases are of genetic origin (mutations described in the genes PARK alpha-synuclein, DJ-1, PINK, LRRK2, etc.) leading to early PD attacks, the majority of cases remain idiopathic and are associated with aging. . In addition to genetic predisposition, associated risk factors include environmental toxins, pesticides, heavy metals, traumatic injuries, and bacterial or viral infections [3], all of which are closely associated with inflammation. The important role of inflammation in the development of parkinsonian symptoms has been suspected for many years since the initial observation of parkinsonian symptoms in individuals infected with influenza virus (lethargic encephalitis) [4]. Subsequently, PD has been associated with several viral pathogens including influenza A, herpes simplex virus 1 (HSV-1), Ebola virus (EBV), varicella-zoster virus, Japanese encephalitis virus, vanilla necrosis virus, and human immunodeficiency virus. virus As with Helicobacter pylori [5]. neurotropic pathogens through the basal ganglia through the nasal mucosa, through the olfactory pathways, and through the intestinal mucosa, through the intestinal plexus and preganglionic vagal fibers, ultimately leading to neuroinflammatory and neurodegenerative cascades [6]. It is interesting that, in addition to eliciting an acute immune response in the nigrostriatal tract, some viral proteins (HSV-1 and EBV) exhibit a molecular interaction with alpha-synuclein (α-Syn) and α-Syn, promoting integration and bringing them together more. . Intracellular deposits are called Lewy bodies [7]. In addition, α-Syn in the enteric nervous system exhibits a potent chemoattractant activity of neutrophils and monocytes in response to viral infection, implicating the protein in systemic and brain inflammatory responses in the pathogenesis of PD [8].

Inflammation is a highly regulated mechanism against pathogenic stimuli or tissue injury that is intended to protect the host from damaging agents and promote tissue repair. The central nervous system (CNS) has long been considered an immune-competent tissue due to its separation from the peripheral immune system by the blood-blood barrier (BBB). But this concept has changed. Indeed, a powerful innate immune response can be elicited in the CNS against pathogen-associated molecular patterns (PAMPs) and associated molecular patterns (DAMPs). Under physiological conditions, microglia and astroglia continuously monitor the brain parenchyma to maintain CNS homeostasis, releasing neurotrophic factors, removing synaptic glutamate, remodeling and reforming synapses, etc. However, these glial cells can be stimulated by the secretion of PAMPS and DAMPS, such as of damaged neurons or protein aggregates, leading to persistent neuroinflammation. Although it may not represent the initiating factor in every case of PD, chronic neuroinflammation appears to be a cofactor in disease development.

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Next, considerable evidence in human samples and animal models supports the involvement of inflammation in the development of PD. However, the exact trigger for this response is unclear. While inflammation may result in ongoing neuronal cell death in PD, it is likely that α-Syn may also play a direct role in dysregulation. In addition to the well-documented brain microgliosis and astrogliosis in PD, peripheral inflammation and PD risk-associated genes support an important contribution of the chronic inflammatory response to the development of this neurodegenerative disease. We will provide a systematic review of the cellular mediators and molecular mechanisms involved in neuroinflammation and how they may influence the development of PD.

Microglia are CNS-resident macrophages, initially described by Pio del Rio Ortega. These cells, in addition to their homeostatic functions, constitute the frontal defense of the innate immune system. These cells secrete neurotrophic factors, remove toxins, and mediate neuronal repair, remodeling, and synaptic pruning [ 11 ]. Analysis of postmortem specimens and neuroimaging implicates microglia in the pathophysiology of PD.

Microglial mobility with multiple functional phenotypes allows a rapid and adaptive response to inflammatory stimuli. Under basal homeostatic conditions, microglia have a basal state of activity, vaguely to a resting state, in which the microenvironment is perceived to sense infection and stress cells and immunomodulatory cell molecules, such as CX3CL1, CD200, CD22, CD45, CD95 or those released by healthy neurons [13]. In response to inflammatory challenges, microglia are functionally polarized to the classic proinflammatory M1 phenotype or the alternative immunosuppressive and cytoprotective (“wound healing”) M2 phenotype [14]. Transcriptomic studies have added further levels of complexity to disease-specific microglial signatures, but these results have yet to be validated [15]. DAMPS fold or aggregate proteins, such as α -Syn, with signals provided by toll receptors. TLRs) for the acquisition of a proinflammatory M1 phenotype by microglia [16, 17, 18]. This phenotype is characterized by large cell body and amoeboid morphology and upregulation of major histocompatibility complex (MHC) I and II molecules [19], and increased production of proinflammatory mediators (cytokines, IL1β, IL6, TNFα, chemokines). and bioactive lipids) [20]. Therefore, M1 microglia can change the permeability of the BBB and induce brain infiltration by circulating leukocytes [21], therefore potentiating the local inflammatory response. In addition, DAMPs released by stressed and dying neurons induce the expression of genes that compose the NADPH oxidase (NOX) system and reactive oxygen species (ROS) and nitric oxide for NOS2 in humans (through NOS1 and NOS3, they produce [” 22 ] ] ), with an antimicrobial function, which together with chronic inflammation [ 23 ]. Negative mechanisms with anti-inflammatory factors (cytokines such as IL4 and IL10, and a new class of mediators of resolution, including lipoxins, resolvins, protectins, and maresins) must act to resolve inflammation under physiological conditions. But this disadvantage in chronic diseases [24]. With the acquisition of the M1 microglial phenotype in PD, elevated levels of IL1β, IL6 and TNFα were detected in the striatum, as well as in postmortem SN specimens [25]. Interestingly, incubation of dopaminergic neurons with conditioned medium from M1 microglia It has been shown that the death cell is favorable, but mixed.

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