Abstract
The aim of this study is to identify and validate protein change in the serum from PD patients. We used serum samples from 21 PD patients and 20 age-matched normal people as control to conduct a comparative proteomic study. We performed 2-DE and analyzed the differentially expressed protein spots by LC-MS/MS. In PD group 13 spots were shown to be differentially expressed compared to control group. They were identified as 6 proteins. Among these, 3 proteins were confirmed by Western blot analysis. It showed that the frequency of fibrinogen γ-chain (FGG) appeared 70% in PD, which could not be detected in control group. The protein of inter-alpha-trypsin inhibitor heavy chain H4 (ITI-H4) was found to exist two forms in serum. The full size (120 kDa) of the protein was increased and the fragmented ITI-H4 (35 kDa) was decreased in PD group. The ratio of full size ITI-H4 to fragmented ITI-H4 in PD patients was 3.85±0.29-fold higher than in control group. Furthermore, fragmented Apo A-IV (∼26 kDa) was mainly detected in control group, while it was rare to be found in PD group. Above findings might be useful for diagnosis of PD. When the expressions of FGG and 120 kDa ITI-H4 are increase, as well as ∼26 kDa Apo A-IV disappear would provide strong evidence for PD.
Highlights
Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease (AD), characterized by progressive and profound loss of neuromelanin containing dopaminergic neurons in the substantia nigra pars compacta (SNpc) with presence of eosinophillic, intracytoplasmic, proteinaceous inclusions termed as Lewy bodies (LB) and dystrophic Lewy neurites in surviving neurons [1]
Some potential protein biomarkers in the blood and cerebrospinal fluid have been pursued for the diagnosis and staging of PD
DJ-1 and a-synuclein, two proteins critically involved in PD pathogenesis, have been tested as potential disease biomarkers, but results have been inconsistent [20], [21]
Summary
Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease (AD), characterized by progressive and profound loss of neuromelanin containing dopaminergic neurons in the substantia nigra pars compacta (SNpc) with presence of eosinophillic, intracytoplasmic, proteinaceous inclusions termed as Lewy bodies (LB) and dystrophic Lewy neurites in surviving neurons [1]. Clinical features of PD include motor impairments involving resting tremor, bradykinesia and rigidity along with non-motoric symptoms like autonomic, cognitive and psychiatric problems. The accurate clinical diagnosis remains challenging [2], [3]. A clinical validation for PD can be time-consuming, with multiple tests including motor, olfactory, visual, and psychological assessments, imaging (MRI, PET), as well as biochemical testing of cerebrospinal fluid (CSF), lung, liver, heart, and lymphocytes [4,5,6]. Mitochondrial, proteasomal dysfunction and oxidative stress are widely recognized as major contributors, the mechanisms underlying the development of PD remain unknown [7], [8]. The discovery of key proteins related to the development and progression of PD would shed greater light on PD pathogenesis, but would provide new targets for drug discovery
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