Regulation of striatal astrocytic receptor for advanced glycation end‐products variants in an early stage of experimental Parkinson's disease

Viana, Sofia D.; Valero, Jorge; Rodrigues-Santos, Paulo; Couceiro, Patrícia; Silva, Andréa M.; Carvalho, Félix; Ali, Syed F.; Ribeiro, Carlos; Pereira, Frederico C.

doi:10.1111/jnc.13682

Cited by 25 publications

(26 citation statements)

References 61 publications

(139 reference statements)

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“…Importantly, it has even been suggested that AGEs might trigger Lewy body formation prior to the onset of PD, since they were found in Lewy bodies in incidental Lewy body disease patients’ brains ( Münch et al, 2000 ; Dalfó et al, 2005 ). Glycation was also reported in several models of parkinsonism, namely the MPTP model of PD ( Teismann et al, 2012 ; Viana et al, 2016 ; Vicente Miranda et al, 2017 ). Interestingly, in toxin-based animal models of PD the depletion of dopaminergic neurons in the SNpc is aggravated in animals that were concomitantly submitted to a high fat diet regimen ( Bousquet et al, 2012 ; Ma et al, 2015 ), suggesting that this diet may increase the susceptibility of animal to PD-inducing drugs.…”

Section: Glycation In Parkinson’s Diseasementioning

confidence: 82%

“…Among those, S100/calgranulin family of proinflammatory cytokine like mediators is a major inducer of RAGE activation ( Hofmann et al, 1999 ; Donato, 2001 ), already reported in neurodegenerative diseases. Interestingly, S100B protein levels are increased in SNpc and CSF from PD patients ( Sathe et al, 2012 ), and in striata from mice submitted to MPTP treatment ( Viana et al, 2016 ). Accordingly, lack of S100B resulted in decreased expression of both RAGE and TNF-α with consequent reduced microglia activation and neuroprotection ( Sathe et al, 2012 ), further implicating S100B/RAGE axis in the neurodegenerative process in PD.…”

Section: Glycation In Parkinson’s Diseasementioning

confidence: 99%

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Linking Glycation and Glycosylation With Inflammation and Mitochondrial Dysfunction in Parkinson’s Disease

Videira

Castro-Caldas

2018

Front. Neurosci.

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Parkinson’s disease (PD) is the second most common neurodegenerative disorder, affecting about 6.3 million people worldwide. PD is characterized by the progressive degeneration of dopaminergic neurons in the Substantia nigra pars compacta, resulting into severe motor symptoms. The cellular mechanisms underlying dopaminergic cell death in PD are still not fully understood, but mitochondrial dysfunction, oxidative stress and inflammation are strongly implicated in the pathogenesis of both familial and sporadic PD cases. Aberrant post-translational modifications, namely glycation and glycosylation, together with age-dependent insufficient endogenous scavengers and quality control systems, lead to cellular overload of dysfunctional proteins. Such injuries accumulate with time and may lead to mitochondrial dysfunction and exacerbated inflammatory responses, culminating in neuronal cell death. Here, we will discuss how PD-linked protein mutations, aging, impaired quality control mechanisms and sugar metabolism lead to up-regulated abnormal post-translational modifications in proteins. Abnormal glycation and glycosylation seem to be more common than previously thought in PD and may underlie mitochondria-induced oxidative stress and inflammation in a feed-forward mechanism. Moreover, the stress-induced post-translational modifications that directly affect parkin and/or its substrates, deeply impairing its ability to regulate mitochondrial dynamics or to suppress inflammation will also be discussed. Together, these represent still unexplored deleterious mechanisms implicated in neurodegeneration in PD, which may be used for a more in-depth knowledge of the pathogenic mechanisms, or as biomarkers of the disease.

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Section: Glycation In Parkinson’s Diseasementioning

confidence: 82%

Section: Glycation In Parkinson’s Diseasementioning

confidence: 99%

Linking Glycation and Glycosylation With Inflammation and Mitochondrial Dysfunction in Parkinson’s Disease

Videira

Castro-Caldas

2018

Front. Neurosci.

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“…Although glycation products may be unaffected in the face of evidence of striatal damage from known dopaminergic neurotoxicants such as MPTP (Viana et al . ), this is not necessarily the case for METH toxicity which involves pronounced hyperthermia and hypertension (unlike MPTP). Also, the vascular damage and neurodegeneration resulting in the parietal cortex and thalamus due to METH exposure may not involve exactly the same mechanisms as neurodegeneration in the other brain regions in which MPTP produces neurotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Corticosterone and exogenous glucose alter blood glucose levels, neurotoxicity, and vascular toxicity produced by methamphetamine

Bowyer

Tranter

Sarkar

et al. 2017

Journal of Neurochemistry

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Our previous studies have raised the possibility that altered blood glucose levels may influence and/or be predictive of methamphetamine (METH) neurotoxicity. This study evaluated the effects of exogenous glucose and corticosterone (CORT) pretreatment alone or in combination with METH on blood glucose levels and the neural and vascular toxicity produced. METH exposure consisted of four sequential injections of 5, 7.5, 10, and 10 mg/kg (2h between injections) D-METH. The three groups given METH in combination with saline, glucose (METH+Glucose), or CORT (METH+CORT) had significantly higher glucose levels compared to the corresponding treatment groups without METH except at 3 h after the last injection. At this last time point, the METH and METH+Glucose groups had lower levels than the non-METH groups, while the METH+CORT group did not. CORT alone or glucose alone did not significantly increase blood glucose. Mortality rates for the METH+CORT (40%) and METH+Glucose (44%) groups were substantially higher than the METH (< 10%) group. Additionally, METH+CORT significantly increased neurodegeneration above all other treatments (≈ 2.5-fold in the parietal cortex). Thus, maintaining elevated levels of glucose during METH exposure increases lethality and may exacerbate neurodegeneration. Neuroinflammation, specifically microglial activation, was associated with degenerating neurons in the parietal cortex and thalamus after METH exposure. The activated microglia in the parietal cortex were surrounding vasculature in most cases and the extent of microglial activation was exacerbated by CORT pretreatment. Our findings implicate elevated blood levels of glucose and hyperthermia in METH-induced neurotoxicity, neurovascular damage, and lethality, and that acute elevation of CORT exacerbates both neurotoxicity and neuroinflammation.

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“…; Viana et al . ). In addition, transgenic mice over‐expressing S100B have been reported to develop features of PD, such as the impairment of motor coordination and the expression of some molecular parameters, including the dopamine‐D2 receptor (Liu et al .…”

Section: S100b As An Active Factor In Neural Injurymentioning

confidence: 97%

“…In the pathogenic mechanisms of PD, a crucial role has been indicated for activated pro-inflammatory astrocytes, also involving the overproduction and release of S100B, in response to striatal dopaminergic denervation or 6-hydroxydopamine administration Morales et al 2016). S100B was over-expressed in crucial brain regions such as substantia nigra and striatum both in PD patients (Sathe et al 2012;Rydbirk et al 2017) and in MPTP-treated mice (Sathe et al 2012;Viana et al 2016). In addition, transgenic mice over-expressing S100B have been reported to develop features of PD, such as the impairment of motor coordination and the expression of some molecular parameters, including the dopamine-D2 receptor (Liu et al 2011).…”

Section: Neurodegenerative Diseasesmentioning

confidence: 99%

The S100B story: from biomarker to active factor in neural injury

Michetti

D’Ambrosi

Toesca

et al. 2018

Journal of Neurochemistry

273

238

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S100B is a Ca -binding protein mainly concentrated in astrocytes. Its levels in biological fluids (cerebrospinal fluid, peripheral and cord blood, urine, saliva, amniotic fluid) are recognized as a reliable biomarker of active neural distress. Although the wide spectrum of diseases in which the protein is involved (acute brain injury, neurodegenerative diseases, congenital/perinatal disorders, psychiatric disorders) reduces its specificity, its levels remain an important aid in monitoring the trend of the disorder. Mounting evidence now points to S100B as a Damage-Associated Molecular Pattern molecule which, when released at high concentration, through its Receptor for Advanced Glycation Endproducts, triggers tissue reaction to damage in a series of different neural disorders. This review addresses this novel scenario, presenting data indicating that S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease: acute brain injury (ischemic/hemorrhagic stroke, traumatic injury), neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis), congenital/perinatal disorders (Down syndrome, spinocerebellar ataxia-1), psychiatric disorders (schizophrenia, mood disorders), inflammatory bowel disease. In many cases, over-expression/administration of the protein induces worsening of the disease, whereas its deletion/inactivation produces amelioration. This review points out that the pivotal role of the protein resulting from these data, opens the perspective that S100B may be regarded as a therapeutic target for these different diseases, which appear to share some common features reasonably attributable to neuroinflammation, regardless their origin.

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Regulation of striatal astrocytic receptor for advanced glycation end‐products variants in an early stage of experimental Parkinson's disease

Cited by 25 publications

References 61 publications

Linking Glycation and Glycosylation With Inflammation and Mitochondrial Dysfunction in Parkinson’s Disease

Linking Glycation and Glycosylation With Inflammation and Mitochondrial Dysfunction in Parkinson’s Disease

Corticosterone and exogenous glucose alter blood glucose levels, neurotoxicity, and vascular toxicity produced by methamphetamine

The S100B story: from biomarker to active factor in neural injury

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