Beyond the boundaries of inflammation in Atypical Parkinsonism

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About this Research Topic

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Background

Atypical parkinsonisms are a group of diseases associated with parkinsonian syndromes generally affected by moderate or lack of response to levodopa treatment. Among them can be mentioned Progressive Supranuclear Palsy (PSP), Corticobasal Syndrome (CBS) and Multiple System Atrophy (MSA). PSP is the most common of them. Additionally PSP is related with various phenotypes often resembling other diseases as Parkinson’s Disease and MSA. The tauopathic parkinsonian syndromes are based on various pathologies. Due to their unspecific clinical manifestation, lack of methods enabling making in vivo definite diagnosis, further exploration regarding examination of these entities is required.

The inflammatory pathogenesis of neurodegenerative disorders remains not fully explored. Since the primary association between HLA-DR-positive microglial activation and neurodegeneration, various concepts regarding the mechanisms in synclueinopathies and tauopathies were introduced. In PSP neuroinflammatory patterns related to pathomechanism were linked with abnormalities regarding such factors as IL-1β and microglial-derived cytokines. It is also unknown whether tauopathy is more a cause or a consequence of the neuroinflammatory activation. The microglial activation may be correlated with neutralization, disintegration or deletion of tau and increase in tau phosphorylation. The microglial-derived cytokines were also found to play a role in multiple system atrophy. The microglial activation was found to remain activated after the destruction of the dopaminergic system. More is known in the neuroinflammatory pathogenesis of Parkinson’s Disease (PD). The pathogenesis of this disease is associated with abnormalities in iron, ferritin and oxidative stress. The levels of inflammatory cytokines and NT-proCNP was also found to show abnormalities. Microglial activation in neurodegenerative diseases was also evaluated in the context of its genetic context and its association CXCL12, TLR2, RALB, CCR5 and CXCR4. The last of the mentioned genes was associated with neurodegeneration in PSP. The goal of this research topic is to elaborate on inflammation as a tool not only applicable in understanding the pathogenesis of atypical parkinsonisms and related disorders, but also to obtain a feasible tool, which would be critical in the differentiation of the entities.

The possible pathogenesis of syndromes associated with atypical parkinsonisms may be also based on vascular or metabolic pathogenesis. Recently cases of vascular PSP and CBS were described. Growing interest is related to the associations between clinical manifestation of tauopathic parkinsonian syndromes and their correlation with hypertension and diabetes. Prediabetes and glycemic variability are considered factors impacting clinical course of the diseases.

Research areas of interest include, but are not limited to:

o Advances in the field of neurodegeneration and its correlations with neuroinflammatory processes and vascular or metabolic pathogenesis.

o Studies on the role of neuroinflammation and vascular pathogenesis in inducing various pathologies.

o Studies concerning the potential impacting on diseases by modifying the evolution of neuroinflammatory processes and other pathophysiological mechanisms leading to parkinsonims

o Clinical neuroimaging studies on the radiotracers associated with microglial activation and metabolic abnormalities

Keywords: PSP, progressive supranuclear palsy, microglial activation, atypical parkinsonisms, neurodegeneration, corticobasal syndrome, CBS

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