带状疱疹并发肩关节运动性麻痹的康复：1例报告

We describe the case of a 73-year-old man with left shoulder paresis caused by a herpes zoster infection of the left C5 dermatomes. The patient had been affected by pain for 10 days, a skin rash on his left shoulder and back for 5 days, and weakness of his left shoulder for 2 days before admission. Electromyography revealed denervation discharges from the left supraspinatus, infraspinatus and deltoid muscles, which was compatible with radiculopathy showing after zoster infection. The patient was examined in accordance with the International Classification of Functioning, Disability and Health, and treated with range-of-movement and strengthening exercises as well as activities of daily living and social participation. At 14 months after the onset of the condition, muscle strength had returned to normal. Electromyography revealed that motor unit action potentials were largely normal. These results indicate that the rehabilitation of paresis caused by herpes zoster can obtain positive results with suitable movement training.     

Digit and letter alexia in carbon monoxide poisoning

This study examined a 24-year-old patient with delayed encephalopathy, who was admitted to hospital with complaints of headache and visual impairment 1 week after acute carbon monoxide poisoning. The results of a visual field assessment, electroencephalography and head magnetic resonance imaging indicated damage to the cerebral cortex. After a 2-week treatment period, the patient had recovered from the visual impairment, but exhibited digit- and letter-reading difficulty. The Chinese aphasia battery and the number and letter battery supplement were conducted. The results revealed that the patient exhibited digit and letter alexia, while the ability to read Chinese characters was preserved. In contrast, the patient exhibited a deficit in Chinese character writing, while number and letter writing remained intact. Following treatment, reading and writing ability was improved and electroencephalographic abnormalities were ameliorated. Overall, our experimental findings demonstrated that delayed encephalopathy following acute carbon monoxide poisoning was characterized by digit and letter alexia.     

Case report of adjunctive use of olanzapine with an antidepressant to treat sleep paralysis

Summary： Sleep paralysis （SP） is a condition of unknown etiology that usually occurs when falling asleep or when awakening in which the individual remains conscious but is unable to control their voluntary movements. This case report is about a 68-year-old man with a 40-year history of symptoms of SP and associated panic attacks upon awakening. Neurological examination and neuroimaging identified no abnormalities. Five years before the current evaluation he had been diagnosed with depression and treated with various anti-depressants which ameliorated, but did not cure, his SP. However, this 40-year history of SP was abruptly terminated - and did not return over the subsequent two years--after adjunctive treatment with 2.5 mg olanzapine each night was added to his antidepressant.     

Preoperative functional MRI localization of language areas in Chinese patients with brain tumors Validation with intraoperative electrocortical mapping

Ten Chinese patients with brain tumors involving language regions were selected.Preoperative functional MRI was performed to locate Broca’s or Wernicke’s area,and the cortex that was essential for language function was determined by electrocortical mapping.A site-by-site comparison between functional MRI and electrocortical mapping was performed with the aid of a neuronavigation device.Results showed that the sensitivity and specificity of preoperative functional MRI were 80.0% and 85.0% in Broca’s area and 66.6% and 85.2% in Wernicke’s area,respectively.These experimental findings indicate that functional MRI is an accurate,reliable technique with which to identify the location of Wernicke’s area or Broca’s area in patients with brain tumors.     

Photosensitivity as a symptom of maladapive plasticity in a patient with traumatic brain injury: Diffusion tensor imaging study

We report on a patient with traumatic brain injury who had photosensitivity as the presenting visual symptom and demonstrated axonal injury of the left optic radiation using diffusion tensor imaging. A 41-year-old man with traumatic brain injury began to complain of photosensitivity about 4 months after head trauma. The ophthalmic evaluation, including visual evoked potential study and conventional brain MRI, did not exhibit a pathologic basis for his photosensitivity. However, we did detect axonal injury in the left optic radiation on a diffusion tensor imaging study 36 months after onset. This lesion was almost recovered on 76-month diffusion tensor imaging study, however, the photosensitivity had continued. We suggest that the photosensitivity in this patient was caused by axonal injury of the left optic radiation and it seems to be a symptom of maladaptive plasticity that occurs during the recovery of the axonal injury of the left optic radiation.     

Wernicke encephalopathy☆ Clinical presentation and MR images in two nonalcoholic patients

The aim of the present study was to investigate the importance of and correlation between clinical presentations and magnetic resonance imaging （MRI） of two different cases of nonalcoholic Wernicke encephalopathy. Case l ： A 63-year-old man with a diagnosis of incomplete mechanical intestinal obstruction. His abdominal symptoms were improved by gastrointestinal decompression, but blurred vision, hypoacusis, dizziness, and unsteady gait were noted. His illness deteriorated to confusion on day seven. MRI showed hyperintense lesions in the medial thalami, tectum of the midbrain, and the periaqueduct region on T2- and diffusion-weighted images. Thiamine therapy was commenced immediately with good results. Case 2： A 22-year-old woman was admitted for sudden-onset confabulation and unsteady gait after hyperemesis gravidarum. She had no history of alcohol or any medication. Brain MRI was normal. The patient experienced relief after Vitamin B1 treatment. These results suggest that brain MRI can define characteristic abnormalities in Wernicke encephalopathy, and that diffusion-weighted imaging may improve the diagnosis sensitivity. In addition, the MRI images may be correlated to the clinical stage and severity of the disease. Nevertheless, the clinical features are essential for correct diagnosis.     

Curcumin protects nigral dopaminergic neurons by iron-chelation in the 6-hydroxydopamine rat model of Parkinson’s disease

Objective Curcumin is a plant polyphenolic compound and a major component of spice turmeric (Curcuma longa). It has been reported to possess free radical-scavenging, iron-chelating, and anti-inflammatory properties in dif- ferent tissues. Our previous study showed that curcumin protects MES23.5 dopaminergic cells from 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in vitro. The present study aimed to explore this neuroprotective effect in the 6-OHDA-lesioned rat model of Parkinson’s disease in vivo. Methods Rats were given intragastric curcumin for 24 days. 6-OHDA lesioning was conducted on day 4 of curcumin treatment. Dopamine content was assessed by high-performance liquid chromatography with electrochemical detection, tyrosine hydroxylase (TH)-containing neurons by immunohistochemistry, and iron-containing cells by Perls’ iron staining. Results The dopamine content in the striatum and the number of TH-immunoreactive neurons decreased after 6-OHDA treatment. Curcumin pretreatment reversed these changes. Further studies demonstrated that 6-OHDA treatment increased the number of iron-staining cells, which was dramatically decreased by curcumin pretreatment. Conclusion The protective effects of curcumin against 6-OHDA may be attributable to the ironchelating activity of curcumin to suppress the iron-induced degeneration of nigral dopaminergic neurons.     

Therapeutic benefit of repetitive transcranial magnetic stimulation for severe mirror movements A case report

Congenital mirror movements retard typical hand functions,but no definite therapeutic modality is available to treat such movements.We report an 8-year-old boy with severe mirror movements of both hands.His mirror movements were assessed using the Woods and Teuber grading scale and his fine motor skills were also evaluated by the Purdue Pegboard Test.A 2-week regimen of repetitive transcranial magnetic stimulation produced markedly diminished mirror movement symptoms and increased the fine motor skills of both hands.Two weeks after the completion of the regimen,mirror movement grades had improved from grade 4 to 1 in both hands and the Purdue Pegboard Test results of the right and left hands also improved from 12 to 14 or 13.These improvements were maintained for 1 month after the 2-week repetitive transcranial magnetic stimulation regimen.After 18 months,the mirror movement grade was maintained and the Purdue Pegboard test score had improved to 15 for the right hand while the left hand score was maintained at 13.This occurred without any additional repetitive transcranial magnetic stimulation or other treatment.These findings suggest that repetitive transcranial magnetic stimulation for this patient had a therapeutic and long-term effect on mirror movements.     

Contralateral C7 transfer combined with acellular nerve allografts seeded with differentiated adipose stem cells for repairing upper brachial plexus injury in rats

Nerve grafting has always been necessary when the contralateral C7 nerve root is transferred to treat brachial plexus injury. Acellular nerve allograft is a promising alternative for the treatment of nerve defects, and results were improved by grafts laden with differentiated adipose stem cells. However, use of these tissue-engineered nerve grafts has not been reported for the treatment of brachial plexus injury. The aim of the present study was to evaluate the outcome of acellular nerve allografts seeded with differentiated adipose stem cells to improve nerve regeneration in a rat model in which the contralateral C7 nerve was transferred to repair an upper brachial plexus injury. Differentiated adipose stem cells were obtained from Sprague-Dawley rats and transdifferentiated into a Schwann cell-like phenotype. Acellular nerve allografts were prepared from 15-mm bilateral sections of rat sciatic nerves. Rats were randomly divided into three groups: acellular nerve allograft, acellular nerve allograft + differentiated adipose stem cells, and autograft. The upper brachial plexus injury model was established by traction applied away from the intervertebral foramen with micro-hemostat forceps. Acellular nerve allografts with or without seeded cells were used to bridge the gap between the contralateral C7 nerve root and C5–6 nerve. Histological staining, electrophysiology, and neurological function tests were used to evaluate the effect of nerve repair 16 weeks after surgery. Results showed that the onset of discernible functional recovery occurred earlier in the autograft group first, followed by the acellular nerve allograft + differentiated adipose stem cells group, and then the acellular nerve allograft group; moreover, there was a significant difference between autograft and acellular nerve allograft groups. Compared with the acellular nerve allograft group, compound muscle action potential, motor conduction velocity, positivity for neurofilament and S100, diameter of regenerating axons, myelin sheath thickness, and density of myelinated fibers were remarkably increased in autograft and acellular nerve allograft + differentiated adipose stem cells groups. These findings confirm that acellular nerve allografts seeded with differentiated adipose stem cells effectively promoted nerve repair after brachial plexus injuries, and the effect was better than that of acellular nerve repair alone. This study was approved by the Animal Ethics Committee of the First Affiliated Hospital of Sun Yat-sen University of China(approval No. 2016-150) in June 2016.     

A case of hereditary multi-infarct dementia Mutation in exon 11 of the Notch3 gene on chromosome 19

This study is a report on one 59-year-old male patient with hereditary multi-infarct dementia who came from a family with a positive family history of this disease.The patient primarily presented with dizziness accompanied by vertigo and a positive Romberg’s sign.Skull magnetic resonance images showed lacunar infarction in bilateral temporal lobes,bilateral basal ganglias,periventricular white matter and semioval center,and ischemic focus accompanied by white matter degeneration,exhib-iting senile morphological brain changes.No abnormalities were observed by skull magnetic reso-nance angiography.Gene detection further confirmed that there was Arg607Cys heterozygous mutation in exon 11 of the Notch3 gene.No other mutations in exons were detected.     

Viability of primary cultured retinal neurons in a hyperglycemic condition

The retina of Wistar rats within 1-3 days of birth were dissociated into a retinal cell suspension using 0.05% trypsin digestion. The cell suspension was incubated in Dulbecco’s modified Eagle’s medium for 24 hours, followed by neurobasal medium for 5-7 days. Nissl staining showed that 79.86% of primary cultured retinal cells were positive and immunocytochemical staining showed that the purity of anti-neurofilament heavy chain antibody-positive cells was 71.53%, indicating that the primary culture system of rat retinal neurons was a reliable and stable cell system with neurons as the predominant cell type. The primary cultured retinal neurons were further treated with 0, 5.5, 15, 25, and 35 mM glucose for 24, 48, and 72 hours. The thiazolyl blue tetrazolium bromide test and flow cytometry showed that with increasing glucose concentration and treatment duration, the viability of retinal neurons was reduced, and apoptosis increased. In particular, 35 mM glucose exhibited the most significant effect at 72 hours. Thus, rat retinal neurons treated with 35 mM glucose for 72 hours can be used to simulate a neuronal model of diabetic retinopathy.     

本期导读(英文)

The first paper in this issue is a review of the use of antipsychotic medications in the treatment of depressive conditions. [1] Previously, combined therapy with antidepressants and antipsychotics was largely a time-limited alternative in patients whose depressive symptoms were complicated by delusions and hallucinations. Several trends over the last two decades have gradually changed the clinical attitude about this issue. The rapid increase in the diagnosis     

Changes in a cerebellar peduncle lesion in a patient with Dandy-Walker malformation A diffusion tensor imaging study

We report a patient with severe ataxia due to Dandy-Walker malformation, who showed functional recovery over 10 months corresponding to a change in a cerebellar peduncle lesion. A 20-month-old female patient who was diagnosed with Dandy-Walker syndrome and six age- and sex-matched healthy control subjects were enrolled. The superior cerebellar peduncle, the middle cerebellar peduncle, and the inferior cerebellar peduncle were evaluated using fractional anisotropy and the apparent diffusion coefficient. The patients’ functional ambulation category was 0 at the initial visit, but improved to 2 at the follow-up evaluation, and Berg’s balance scale score also improved from 0 to 7. Initial diffusion tensor tractography revealed that the inferior cerebellar peduncle was not detected, that the fractional anisotropy of the superior cerebellar peduncle and middle cerebellar peduncle decreased by two standard deviations below, and that the apparent diffusion coefficient increased by two standard deviations over normal control values. However, on follow-up diffusion tensor tractography, both inferior cerebellar peduncles could be detected, and the fractional anisotropy of superior cerebellar peduncle increased to within two standard deviations of normal controls. The functional improvement in this patient appeared to correspond to changes in these cerebellar peduncles. We believe that evaluating cerebellar peduncles using diffusion tensor imaging is useful in cases when a cerebellar peduncle lesion is suspected.     

Brain-derived neurotrophic factor mediates macrophage migration inhibitory factor to protect neurons against oxygen-glucose deprivation

Macrophage migration inhibitory factor(MIF)is a chemokine that plays an essential role in immune system function.Previous studies suggested that MIF protects neurons in ischemic conditions.However,few studies are reported on the role of MIF in neurological recovery after ischemic stroke.The purpose of this study is to identify the molecular mechanism of neuroprotection mediated by MIF.Human neuroblastoma cells were incubated in Dulbecco’s modified Eagle’s medium under oxygen-glucose deprivation(OGD)for 4 hours and then returned to normal aerobic environment for reperfusion(OGD/R).30 ng/mL MIF recombinant(30 ng/mL)or ISO-1(MIF antagonist;50μM)was administered to human neuroblastoma cells.Then cell cultures were assigned to one of four groups:control,OGD/R,OGD/R with MIF,OGD/R with ISO-1.Cell viability was analyzed using WST-1 assay.Expression levels of brain-derived neurotrophic factor(BDNF),microtubule-associated protein 2(MAP2),Caspase-3,Bcl2,and Bax were detected by western blot assay and immunocytochemistry in each group to measure apoptotic activity.WST-1 assay results revealed that compared to the OGD/R group,cell survival rate was significantly higher in the OGD/R with MIF group and lower in the OGD/R with ISO-1 group.Western blot assay and immunocytochemistry results revealed that expression levels of BDNF,Bcl2,and MAP2 were significantly higher,and expression levels of Caspase-3 and Bax were significantly lower in the MIF group than in the OGD/R group.Expression levels of BDNF,Bcl2,and MAP2 were significantly lower,and expression levels of Caspase-3 and Bax were significantly higher in the ISO-1 group than in the OGD/R group.MIF administration promoted neuronal cell survival and induced high expression levels of BDNF,MAP2,and Bcl2(anti-apoptosis)and low expression levels of Caspase-3 and Bax(pro-apoptosis)in an OGD/R model.These results suggest that MIF administration is effective for inducing expression of BDNF and leads to neuroprotection of neuronal cells against hypoxic injury.     

猫慢性视神经压迫性损伤模型的构建

BACKGROUND： An animal model of chronic optic nerve injury is necessary to further understand the pathological mechanisms involved. OBJECTIVE： To establish a stabilized, chronic, optic nerve crush model, which is similar to the clinical situation to explore histopathological and optic electrophysiological changes involved in this injury. DESIGN, TIME AND SETTING： A randomized and controlled animal trial was performed at Shanghai Institute of Neurosurgery from May to October 2004, MATERIALS： A BAL3XRAY undetachable balloon and Magic-BD catheter were provided by BLAT, France; JX-2000 biological signal processing system by Second Military Medical University of Chinese PLA, China; inverted phase contrast microscopy by Olympus, Japan. METHODS： A total of twenty normal adult cats were randomly assigned to control （n = 5） and model （n = 15） groups, according to different doses of contrast agent injected through balloons as follows： 0.2 mL injection, 0.25 mL injection, and 0.35 mL injection, with each group containing 5 animals. Imitating the clinical pterion approach, the optic nerves were exposed using micro-surgical methods. An engorged undetachable balloon was implanted beneath the nerve and connected to a catheter. Balloon size was controlled with a contrast agent injection （0.1 mL/10 min） to form an occupying lesion model similar to sellar tumors. MAIN OUTCOME MEASURES： The visually evoked potential examination was used to study optical electrophysiology changes in pre-post chronic optical nerve injury. Ultrastructural pathological changes to the optic nerve were analyzed by electron microscopy. RESULTS： During the early period （day 11 after modeling）, visually evoked potential demonstrated no significant changes. In the late period （day 51 after modeling）, recorded VEP demonstrated that P1 wave latency was prolonged and P1 wave amplitude was obviously reduced. Following injury, the endoneurium, myelin sheath, lamella, axolemma, and axon appeared disordered. CONCLUSION： Results demonstrated that the chronic, intracranial, optical nerve crush model was stable and could simulate optic nerve lesions induced by sellar tumors. Under the condition of chronic optical nerve crush, visually evoked potentials were aggravated.     

Combination of olfactory ensheathing cells and human umbilical cord mesenchymal stem cell-derived exosomes promotes sciatic nerve regeneration

Olfactory ensheathing cells(OECs)are promising seed cells for nerve regeneration.However,their application is limited by the hypoxic environment usually present at the site of injury.Exosomes derived from human umbilical cord mesenchymal stem cells have the potential to regulate the pathological processes that occur in response to hypoxia.The ability of OECs to migrate is unknown,especially in hypoxic conditions,and the effect of OECs combined with exosomes on peripheral nerve repair is not clear.Better understanding of these issues will enable the potential of OECs for the treatment of nerve injury to be addressed.In this study,OECs were acquired from the olfactory bulb of Sprague Dawley rats.Human umbilical cord mesenchymal stem cell-derived exosomes(0–400μg/mL)were cultured with OECs for 12–48 hours.After culture with 400μg/mL exosomes for 24 hours,the viability and proliferation of OECs were significantly increased.We observed changes to OECs subjected to hypoxia for 24 hours and treatment with exosomes.Exosomes significantly promoted the survival and migration of OECs in hypoxic conditions,and effectively increased brain-derived neurotrophic factor gene expression,protein levels and secretion.Finally,using a 12 mm left sciatic nerve defect rat model,we confirmed that OECs and exosomes can synergistically promote motor and sensory function of the injured sciatic nerve.These findings show that application of OECs and exosomes can promote nerve regeneration and functional recovery.This study was approved by the Institutional Ethical Committee of the Air Force Medical University,China(approval No.IACUC-20181004)on October 7,2018;and collection and use of human umbilical cord specimens was approved by the Ethics Committee of the Linyi People’s Hospital,China(approval No.30054)on May 20,2019.     

20S proteasome and glyoxalase 1 activities decrease in erythrocytes derived from Alzheimer’s disease patients

As a result of accumulating methylglyoxal and advanced glycation end products in the brains of patients with Alzheimer’s disease,it is considered a protein precipitation disease.The ubiquitin proteasome system is one of the most important mechanisms for cells to degrade proteins,and thus is very important for maintaining normal physiological function of the nervous system.This study recruited 48 individuals with Alzheimer’s disease(20 males and 28 females aged 75±6 years)and 50 healthy volunteers(21 males and 29 females aged 72±7 years)from the Affiliated Hospital of Youjiang Medical University for Nationalities(Baise,China)between 2014 and 2017.Plasma levels of malondialdehyde and H2O2 were measured by colorimetry,while glyoxalase 1 activity was detected by spectrophotometry.In addition,20S proteasome activity in erythrocytes was measured with a fluorescent substrate method.Ubiquitin and glyoxalase 1 protein expression in erythrocyte membranes was detected by western blot assay.The results demonstrated that compared with the control group,patients with Alzheimer’s disease exhibited increased plasma malondialdehyde and H2O2 levels,and decreased glyoxalase 1 activity;however,expression level of glyoxalase 1 protein remained unchanged.Moreover,activity of the 20S proteasome was decreased and expression of ubiquitin protein was increased in erythrocytes.These findings indicate that proteasomal and glyoxalase activities may be involved in the occurrence of Alzheimer’s disease,and erythrocytes may be a suitable tissue for Alzheimer’s disease studies.This study was approved by the Ethics Committee of Youjiang Medical University for Nationalities(approval No.YJ12017013)on May 3,2017.     

Visual acuity evaluated by pattern-reversal visual-evoked potential is affected by check size/visual angle

Objective To systemically explore the range of visual angles that affect visual acuity,and to establish the relationship between the P1 component(peak latency～100 ms) of the pattern-reversal visual-evoked potential(PRVEP) and the visual acuity at particular visual angles.Methods Two hundred and ten volunteers were divided into seven groups, according to visual acuity as assessed by the standard logarithmic visual acuity chart(SLD-II).For each group,the PRVEP components were elicited in response to visual angle presentations at 8°,4°,2°,1°/60′30’,15’,and 7.5’,in the whiteblack chess-board reversal mode with a contrast level of 100%at a frequency of 2 Hz.Visual stimuli were presented monocularly, and 200 presentations were averaged for each block of trials.The early and stable component P1 was recorded at the mid-line of the occipital region(Oz) and analyzed with SPSS 13.00.Results(1) Oz had the maximum PI amplitude; there was no significant difference between genders or for interocular comparison in normal controls and subjects with optic myopia.(2) The P1 latency decreased slowly below 30’,then increased rapidly.The P1 amplitude initially increased with check size,and was maximal at～1°and～30’.(3) The PI latency in the group with visual acuity≤0.2 was significantly different at 8°,15’ and 7.5’,while the amplitude differed at all visual angles,compared with the group with normal vision.Differences in P1 for the groups with 0.5 and 0.6 acuity were only present at visual angles <1°.(4) Regression analysis showed that the P1 latency and amplitude were associated with visual acuity over the full range of visual angles. There was a moderate correlation at visual angles <30’.Regression equations were calculated for the P1 components and visual acuity,based on visual angle.Conclusion(1) Visual angle should be taken into consideration when exploring the function of the visual pathway,especially visual acuity.A visual angle -60’ might be appropriate when using PRVEP components to evaluate poor vision and to identify malingerers.(2) Increased P1 amplitude and decreased P1 latency were associated with increasing visual acuity,and the P1 components displayed a linear correlation with visual acuity,especially in the range of optimal visual angles.Visual acuity can be deduced from P1 based on visual angle.     

中国大陆脊髓小脑型共济失调三型/马查多-约瑟夫病女性患者的产前诊断：个案报告

Spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD) is a progressive, currently untreatable and ultimately fatal ataxic disorder that belongs to the group of neurological disorders known as CAG-repeat or polyglutamine diseases. Here, we present the first prenatal diagnosis of SCA3/MJD in mainland China in a woman who was known to carry an expanded CAG-trinucleotide repeat in the MJD1 gene. After evaluating motivation and psychological tolerance of the couple, amniocentesis was performed after 14 weeks of gestation. Polymerase chain reactions followed by T-vector cloning and direct sequencing were employed to evaluate the CAG-repeat number of the fetal MJD1 gene. We identified a truncated CAG expansion of 78 repeats in the MJD1 gene of the fetus compared with 81 repeats in his mother.     

cDNA cloning, prokaryotic expression and purification of rat α-synudein

Objective To clone the cDNA of rat α-Syn gene, investigate its prokaryotic expression and produce purified recombinant rat α-Syn protein. Methods Rat α-Syn cDNA was amplified from the rat brain total RNA by RT-PCR and was cloned into pGEX-4T-1, a prokaryotic expressing vector. The recombinant plasmid containing rat α-Syn gene was transformed into E. Coli BL21 to express a fusion protein with rat α-Syn protein tagged by glutathione-S-transferase （GST）. The fusion protein was then cleaved by thrombin during passing through the GST-agarose 4B column to release the recombinant rat α-Syn protein. The recombinant rat a-Syn protein was further purified using Superdex S200 gel filtration. Results DNA sequencing confirmed that the cloned cDNA contained 420 base pairs encoding 140 amino acids, which was identical to the reported amino acid sequence of rat α-Syn. After transformation, the recombinant plasmid pGEX-ra-Syn expressed a soluble protein that was inducible by IPTG. The purified recombinant protein was shown to be single band on SDS-PAGE, with a molecular size of around 18000, which was identical to the reported molecular size of rat α-Syn. Western blot analysis demonstrated that the recombinant protein was recognized by specific antibody against α-Syn. Conclusion The rat α-Syn gene was successfully expressed in prokaryotic expression system and highly purified rat α-Syn recombinant protein was produced.