Altered Regulation of CD200 Receptor in Monocyte-Derived Macrophages from Individuals with Parkinson’s Disease

Luo, Xiaoguang; Zhang, Ji-Juan; Zhang, Chaodong; Liu, Rong; Zheng, Lan; Wang, Xijin; Chen, Shengdi; Ding, Jingzhong

doi:10.1007/s11064-009-0094-6

Cited by 38 publications

(25 citation statements)

References 42 publications

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“…[248] Macrophages from PD patients have also shown reduced CD200 receptors. [138] Reductions in CD200 have also been reported with aging in rats. [140] Since CD200 receptors on microglia are considered major players in microglial switching from a neurodestructive mode to a neuroreparative mode, this could explain prolonged priming/activation of microglia in neurodegenerative disorders [Figure 8].…”

Section: The Aging Brain and Chronic Traumatic Encephalopathymentioning

confidence: 99%

Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis

Blaylock

Maroon²

2011

Surg Neurol Int

188

180

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Some individuals suffering from mild traumatic brain injuries, especially repetitive mild concussions, are thought to develop a slowly progressive encephalopathy characterized by a number of the neuropathological elements shared with various neurodegenerative diseases. A central pathological mechanism explaining the development of progressive neurodegeneration in this subset of individuals has not been elucidated. Yet, a large number of studies indicate that a process called immunoexcitotoxicity may be playing a central role in many neurodegenerative diseases including chronic traumatic encephalopathy (CTE). The term immunoexcitotoxicity was first coined by the lead author to explain the evolving pathological and neurodevelopmental changes in autism and the Gulf War Syndrome, but it can be applied to a number of neurodegenerative disorders. The interaction between immune receptors within the central nervous system (CNS) and excitatory glutamate receptors trigger a series of events, such as extensive reactive oxygen species/reactive nitrogen species generation, accumulation of lipid peroxidation products, and prostaglandin activation, which then leads to dendritic retraction, synaptic injury, damage to microtubules, and mitochondrial suppression. In this paper, we discuss the mechanism of immunoexcitotoxicity and its link to each of the pathophysiological and neurochemical events previously described with CTE, with special emphasis on the observed accumulation of hyperphosphorylated tau.

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Section: The Aging Brain and Chronic Traumatic Encephalopathymentioning

confidence: 99%

Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis

Blaylock

Maroon²

2011

Surg Neurol Int

188

180

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“…Monocyte-derived macrophages (MDMs) from young and old controls were compared with those from PD patients for changes in CD200R expression [64]. Although constitutive CD200R levels were the same between all of the groups, MDMs from PD cases had impaired induction of CD20 OR expression in response to different inflammatory stimuli.…”

Section: Neurobiology Of Cd200 and The Cd200r In Humansmentioning

confidence: 99%

Understanding the Neurobiology of Cd200 and the Cd200 Receptor: A Therapeutic Target For Controlling Inflammation In Human Brains?

Walker

Lue

2013

Future Neurol.

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CD200 and its receptor, CD200 receptor (CD200R), have uniaue roles in controlling damaging inflammatory processes. At present, the only identified function for CD200 is as a ligand for CD200R. These proteins interact resulting in the activation of anti-inflammatory signaling by CD200R-expressing cells. When this interaction becomes deficient with aging or disease, chronic inflammation occurs, Experimental animal studies have demonstrated the consequences of disrupting CD200–CD200R interactions in the brain, but there have been few studies in human brains. Deficiency in neuronal CD200 may explain the chronic inflammation in human neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and multiple sclerosis; however, deficits in the microglial expression of CD200R may also be of functional significance. The purpose of this review is to assess the data regarding the role of CD200–CD200R interactions in relation to the brain in order to determine if this could be a therapeutic target for human brain diseases with inflammatory components, and what additional studies are needed.

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“…Markers such as CD200 and intercellular adhesion molecule-1 (ICAM-1) also reflect inflammatory changes (Wang et al, 2011) and can be readily measured. Both CD200 and ICAM-1 have been studied in relation to neuroinflammation in AD (Akiyama et al, 1993; Frohman et al, 1991; Verbeek et al, 1994; Walker et al, 2009; Zhang et al, 2005) and PD (Luo et al, 2010, Miklossy et al, 2006). Both proteins share similar structures, but have opposite functions.…”

Section: Introductionmentioning

confidence: 99%

Changes in CD200 and intercellular adhesion molecule-1 (ICAM-1) levels in brains of Lewy body disorder cases are associated with amounts of Alzheimer's pathology not α-synuclein pathology

Walker

Lue

Tang

et al. 2017

Neurobiology of Aging

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Enhanced inflammation has been associated with Alzheimer’s disease (AD) and diseases with Lewy body (LB) pathology, such as Parkinson’s disease (PD) and Dementia with Lewy bodies (DLB). One issue is whether amyloid and tangle pathology, features of AD, or α-synuclein LB pathology have similar or different effects on brain inflammation. An aim of this study was to examine if certain features of inflammation changed in brains with increasing LB pathology. To assess this, we measured levels of the anti-inflammatory protein CD200 and the pro-inflammatory protein intercellular adhesion molecule-1 (ICAM-1) in cingulate and temporal cortex from a total of 143 cases classified according to the Unified Staging System for LB disorders. Changes in CD200 and ICAM-1 levels did not correlate with LB pathology, but with AD pathology. CD200 negatively correlated with density of neurofibrillary tangles, phosphorylated tau and amyloid plaque density. ICAM-1 positively correlated with these AD pathology measures. Double immunohistochemistry for phosphorylated α-synuclein and markers for microglia showed limited association of microglia with LB pathology, but microglia strongly associated with amyloid plaques or phosphorylated tau. These results suggest that there are different features of inflammatory pathology in diseases associated with abnormal α-synuclein compared to AD.

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Altered Regulation of CD200 Receptor in Monocyte-Derived Macrophages from Individuals with Parkinson’s Disease

Cited by 38 publications

References 42 publications

Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis

Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis

Understanding the Neurobiology of Cd200 and the Cd200 Receptor: A Therapeutic Target For Controlling Inflammation In Human Brains?

Changes in CD200 and intercellular adhesion molecule-1 (ICAM-1) levels in brains of Lewy body disorder cases are associated with amounts of Alzheimer's pathology not α-synuclein pathology

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