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12 March 2014, Volume 9 Issue 5 Previous Issue    Next Issue

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Technical comments on rodent spinal cord injuries models Zoe Zhang, Yi Ping Zhang, Lisa B. E. Shields, Christopher B. Shields 2014, 9 (5):  453-455.  doi: 10.4103/1673-5374.130052 Abstract ( 264 )   PDF (243KB) ( 1058 )   Save Animal models are required to investigate mechanisms of spinal cord injuries (SCI) and to gain insight into potential treatments. This article describes several experimental animal models that mimic the clinical picture of SCI. Advantages and disadvantages of each method are compared.  Common technical errors in creating experimental SCI are reviewed including poor vertebral stabilization and variability in segmental location. The creation of reliable models of SCI is essential to avoid erroneous outcomes in the laboratory. Prevention of such errors in experimental rodent models may avoid costly and time-consuming clinical trials from being performed. References | Related Articles | Metrics

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Ligaments disruption: a new perspective in the prognosis of spinal cord injury Rafael Martinez-Perez, Luis Jimenez-Roldan, Alfonso Lagares 2014, 9 (5):  456-457.  doi: 10.4103/1673-5374.130053 Abstract ( 225 )   PDF (174KB) ( 852 )   Save Worldwide prevalence of Spinal Cord Injury (SCI) is ranging from 233 to 755 per million inhabitants, whereas reported incidence lies between 10.4 and 83 per million inhabitants per year. Thus, the socioeconomic impact of SCI associated with cervical trauma is high enough to be encountered within one of the most important worries in vast majority of developed countries. The ability to predict recovery following SCI is of paramount importance to the physician’s role in providing the best care and guidance to patients and families during the illness. Diagnosis of cervical spine injury is an essential aspect of the trauma evaluation. This task is especially difficult in patients whose clinical examination is not reliable due to distracting painful injuries, intoxication, or concomitant head injury. For this population the use of radiological imaging is essential. Related Articles | Metrics

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Effect of microenvironment modulation on stem cell therapy for spinal cord injury pain Sufang Liu, Changsheng Li, Ying Xing, Feng Tao 2014, 9 (5):  458-459.  doi: 10.4103/1673-5374.130057 Abstract ( 311 )   PDF (140KB) ( 742 )   Save Transient ischemic attack (TIA) is a temporary event, which portends a higher risk of a disabling stroke following the TIA. However, the evaluation and management of TIA vary worldwide and is debated and controversial. Dr. Mohamed Al-Khaled from University of Lübeck in Germany considered With the development of brain imaging, particularly diffusion weighted imaging-magnetic resonance imaging (DWI-MRI), the diagnosis of TIA changed from time-based definition to a tissue-based one. DWI-MRI became a mandatory tool in the TIA workup. The DWI-MRI provides not only the evidence to distinguish between TIA and acute ischemic stroke, furthermore it predicts TIA patients who are at higher risk of disabling stroke, which can be prevented by an immediate evaluation and treatment of TIA These findings, published in the Neural Regeneration Research (Vol. 9, No. 3, 2014). Related Articles | Metrics

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Extrinsic inhibitors in axon sprouting and functional recovery after spinal cord injury Jessica M. Meves, Binhai Zheng 2014, 9 (5):  460-461.  doi: 10.4103/1673-5374.130056 Abstract ( 374 )   PDF (173KB) ( 1642 )   Save Recovery from injury to the CNS is limited, which is due in large part to the inability of axons to grow after injury. Unfortunately few experimental manipulations have been found that promote regeneration of damaged axons and functional recovery from injury. Nonetheless, targeting various axon growth inhibitors present in the CNS environment promotes compensatory growth of undamaged axons and functional recovery from experimental CNS injury, revealing an alternative approach to promoting functional recovery in patients. Related Articles | Metrics

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Repairing the injured spinal cord: sprouting versus regeneration. Is this a realistic match? Karim Fouad, Caitlin Hurd 2014, 9 (5):  462-462.  doi: 10.4103/1673-5374.130059 Abstract ( 243 )   PDF (111KB) ( 916 )   Save Related Articles | Metrics

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Apolipoprotein E mimetic peptide protects against diffuse brain injury Yaning Zhao, Jianmin Li, Qiqun Tang, Junling Gao, Changxiang Chen, Liwei Jing, Pan Zhang, Shuxing Li 2014, 9 (5):  463-473.  doi: 10.4103/1673-5374.130060 Abstract ( 201 )   PDF (2831KB) ( 1015 )   Save Apolipoprotein E plays a crucial role in inhibiting chronic neurodegenerative processes. However, its impact on neurological function following diffuse brain injury is still unclear. This study was designed to evaluate the therapeutic effects and mechanisms of action of apolipoprotein E mimetic peptide on diffuse brain injury. Apolipoprotein E mimetic peptide was administered into the caudal vein of rats with diffuse brain injury  before and after injury. We found that apolipoprotein E mimetic peptide significantly decreased the number of apoptotic neurons, reduced extracellular signal-regulated kinase1/2 phosphorylation, down-regulated Bax and cytochrome c expression, decreased malondialdehyde content, and increased superoxide dismutase activity in a dose-dependent manner. These experimental findings demonstrate that apolipoprotein E mimetic peptide improves learning and memory function and protects against diffuse brain injury-induced apoptosis by inhibiting the extracellular signal-regulated kinase1/2-Bax mitochondrial apoptotic pathway. Related Articles | Metrics

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Geniposide, the component of the Chinese herbal formula Tongluojiunao, protects amyloid-β peptide (1–42)-mediated death of hippocampal neurons via the non-classical estrogen signaling pathway Jiao Li, Feng Wang, Haimin Ding, Chunyan Jin, Jinyan Chen, Yanan Zhao, Xiaojing Li, Wenju Chen, Ping Sun, Yan Tan, Qi Zhang, Xu Wang, Angran Fan, Qian Hua 2014, 9 (5):  474-480.  doi: 10.4103/1673-5374.130063 Abstract ( 200 )   PDF (541KB) ( 1288 )   Save Tongluojiunao (TLJN) is an herbal medicine consisting of two main components, geniposide and ginsenoside Rg1. TLJN has been shown to protect primary cultured hippocampal neurons. However, its mechanism of action remains unclear. In the present study, primary cultured hippocampal neurons treated with Aβ1–42 (10 µmol/L) significantly increased the release of lactate dehydrogenase, which was markedly reduced by TLJN (2 µL/mL), specifically by the component geniposide (26 µmol/L), but not ginsenoside Rg1 (2.5 µmol/L). The estrogen receptor inhibitor, ICI182780 (1 µmol/L), did not block TLJN- or geniposide-mediated decrease of lactate dehydrogenase under Aβ1–42-exposed conditions. However, the phosphatidyl inositol 3-kinase or mitogen-activated protein kinase pathway inhibitor, LY294002 (50 µmol/L) or U0126 (10 µmol/L), respectively blocked the decrease of lactate dehydrogenase mediated by TLJN or geniposide. Therefore, these results suggest that the non-classical estrogen pathway (i.e., phosphatidyl inositol 3-kinase or mitogen-activated protein kinase) is involved in the neuroprotective effect of TLJN, specifically its component, geniposide, against Aβ1–42-mediated cell death in primary cultured hippocampal neurons. References | Related Articles | Metrics

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rAAV/ABAD-DP-6His attenuates oxidative stress-induced injury of PC12 cells Mingyue Jia, Mingyu Wang, Yi Yang, Yixin Chen, Dujuan Liu, Xu Wang, Lei Song, Jiang Wu, Yu Yang 2014, 9 (5):  481-488.  doi: 10.4103/1673-5374.130065 Abstract ( 256 )   PDF (691KB) ( 1262 )   Save Our previous studies have revealed that amyloid β (Aβ)-binding alcohol dehydrogenase (ABAD) decoy peptide antagonizes Aβ42-induced neurotoxicity. However, whether it improves oxidative stress injury remains unclear. In this study, a recombinant adenovirus constitutively secreting and expressing Aβ-ABAD decoy peptide (rAAV/ABAD-DP-6His) was successfully constructed. Our results showed that rAAV/ABAD-DP-6His increased superoxide dismutase activity in hydrogen peroxide-induced oxidative stress-mediated injury of PC12 cells. Moreover, rAAV/ABAD-DP-6His decreased malondialdehyde content, intracellular Ca2+ concentration, and the level of reactive oxygen species. rAAV/ABAD-DP-6His maintained the stability of the mitochondrial membrane potential. In addition, the ATP level remained constant, and apoptosis was reduced. Overall, the results indicate that rAAV/ABAD-DP-6His generates the fusion peptide, Aβ-ABAD decoy peptide, which effectively protects PC12 cells from oxidative stress injury induced by hydrogen peroxide, thus exerting neuroprotective effects. Related Articles | Metrics

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Shuganjieyu capsule increases neurotrophic factor expression in a rat model of depression Jinhua Fu, Yingjin Zhang, Renrong Wu, Yingjun Zheng, Xianghui Zhang, Mei Yang, Jingping Zhao, Yong Liu 2014, 9 (5):  489-497.  doi: 10.4103/1673-5374.130067 Abstract ( 298 )   PDF (1392KB) ( 2030 )   Save Shuganjieyu capsule has been approved for clinical treatment by the State Food and Drug Administration of China since 2008. In the clinic, Shuganjieyu capsule is often used to treat mild to moderate depression. In the rat model of depression established in this study, Shuganjieyu capsule was administered intragastrically daily before stress. Behavioral results confirmed that depressive symptoms lessened after treatment with high-dose (150 mg/kg) Shuganjieyu capsule. Immunohistochemistry results showed that high-dose Shuganjieyu capsule significantly increased phosphorylation levels of phosphorylation cyclic adenosine monophosphate response element binding protein and brain-derived neurotrophic factor expression in the medial prefrontal cortex and hippocampal CA3 area. Overall, our results suggest that in rats, Shuganjieyu capsule effectively reverses depressive-like behaviors by increasing expression levels of neurotrophic factors in the brain. References | Related Articles | Metrics

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Unusual neural connection between injured cingulum and brainstem in a patient with subarachnoid hemorrhage Jeong Pyo Seo, Sung Ho Jang 2014, 9 (5):  498-499.  doi: 10.4103/1673-5374.130068 Abstract ( 215 )   PDF (775KB) ( 619 )   Save Related Articles | Metrics

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Neuronal activation by acupuncture at Yongquan (KI1) and sham acupoints in patients with disorder of consciousness: a positron emission tomography study Hao Zhang, Xinting Sun, Sujuan Liu, Yingmao Chen, Feng Ling 2014, 9 (5):  500-501.  doi: 10.4103/1673-5374.130070 Abstract ( 255 )   PDF (334KB) ( 777 )   Save Related Articles | Metrics

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Pro-urokinase promotes angiogenesis but does not reduce neuronal apoptosis in infarcted cerebral tissue Wei Qin, Lei Yang, Hongmei Guo, Ning Xiang, Wenli Hu 2014, 9 (5):  502-503.  doi: 10.4103/1673-5374.130072 Abstract ( 254 )   PDF (907KB) ( 809 )   Save References | Related Articles | Metrics

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Recombinant adenovirus-mediated overexpression of 3β-hydroxysteroid-Δ24 reductase Xiuli Lu, Dan Jia, Chenguang Zhao, Weiqi Wang, Ting Liu, Shuchao Chen, Xiaoping Quan, Deliang Sun, Bing Gao 2014, 9 (5):  504-512.  doi: 10.4103/1673-5374.130074 Abstract ( 200 )   PDF (2880KB) ( 958 )   Save 3β-Hydroxysteroid-Δ24 reductase (DHCR24) is a multifunctional enzyme that localizes to the endoplasmic reticulum and has neuroprotective and cholesterol-synthesizing activities. DHCR24 overexpression confers neuroprotection against apoptosis caused by amyloid β deposition. The present study aimed to construct two recombinant adenoviruses driving DHCR24 expression specifically in neurons. Two SYN1 promoter DNA fragments were obtained from human (h) and rat (r). Recombinant Ad-r(h)SYN1-DHCR24 was transfected into AD-293, N2A (mouse neuroblastoma), and MIN6 (mouse pancreatic carcinoma) cells. Western blot analysis showed DHCR24 was specially expressed in 293 and N2A cells, but no specific band was found in MIN6 cells. This demonstrates that the recombinant adenoviruses successfully express DHCR24, and no expression is observed in non-neuronal cells. TUNEL assay results showed apoptosis was inhibited in adenovirus-transfected neurons. Detecting reactive oxygen species by immunofluorescence, we found that adenovirus transfection inhibits apoptosis through scavenging excess reactive oxygen species. Our findings show that the recombinant DHCR24 adenoviruses induce neuron-specific DHCR24 expression, and thereby lay the foundation for further studies on DHCR24 gene therapy for Alzheimer’s disease. Related Articles | Metrics

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Negative regulation of miRNA-9 on oligodendrocyte lineage gene 1 during hypoxic-ischemic brain damage Lijun Yang, Hong Cui, Ting Cao 2014, 9 (5):  513-518.  doi: 10.4103/1673-5374.130077 Abstract ( 176 )   PDF (1776KB) ( 919 )   Save Oligodendrocyte lineage gene 1 plays a key role in hypoxic-ischemic brain damage and myelin repair. miRNA-9 is involved in the occurrence of many related neurological disorders. Bioinformatics analysis demonstrated that miRNA-9 complementarily, but incompletely, bound oligodendrocyte lineage gene 1, but whether miRNA-9 regulates oligodendrocyte lineage gene 1 remains poorly understood. Whole brain slices of 3-day-old Sprague-Dawley rats were cultured and divided into four groups: control group; oxygen-glucose deprivation group (treatment with 8% O2 + 92% N2 and sugar-free medium for 60 minutes); transfection control group (after oxygen and glucose deprivation for 60 minutes, transfected with control plasmid) and miRNA-9 transfection group (after oxygen and glucose deprivation for 60 minutes, transfected with miRNA-9 plasmid). From the third day of transfection, and with increasing culture days, oligodendrocyte lineage gene 1 expression increased in each group, peaked at 14 days, and then decreased at 21 days. Real-time quantitative PCR results, however, demonstrated that oligodendrocyte lineage gene 1 expression was lower in the miRNA-9 transfection group than that in the transfection control group at 1, 3, 7, 14, 21 and 28 days after transfection. Results suggested that miRNA-9 possibly negatively regulated oligodendrocyte lineage gene 1 in brain tissues during hypoxic-ischemic brain damage. References | Related Articles | Metrics

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Transient axonal glycoprotein-1 induces apoptosis-related gene expression without triggering apoptosis in U251 glioma cells Haigang Chang, Shanshan Song, Zhongcan Chen, Yaxiao Wang, Lujun Yang, Mouxuan Du, Yiquan Ke, Ruxiang Xu, Baozhe Jin, Xiaodan Jiang 2014, 9 (5):  519-525.  doi: 10.4103/1673-5374.130079 Abstract ( 189 )   PDF (731KB) ( 1360 )   Save Previous studies show that transient axonal glycoprotein-1, a ligand of amyloid precursor protein, increases the secretion of amyloid precursor protein intracellular domain and is involved in apoptosis in Alzheimer’s disease. In this study, we examined the effects of transient axonal glycoprotein-1 on U251 glioma cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that transient axonal glycoprotein-1 did not inhibit the proliferation of U251 cells, but promoted cell viability. The terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed that transient axonal glycoprotein-1 did not induce U251 cell apoptosis. Real-time PCR revealed that transient axonal glycoprotein-1 substantially upregulated levels of amyloid precursor protein intracellular C-terminal domain, and p53 and epidermal growth factor receptor mRNA expression. Thus, transient axonal glycoprotein-1 increased apoptosis-related gene expression in U251 cells without inducing apoptosis. Instead, transient axonal glycoprotein-1 promoted the proliferation of these glioma cells. References | Related Articles | Metrics

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Increased expression of Notch1 in temporal lobe epilepsy: animal models and clinical evidence Xijin Liu, Zhiyong Yang, Yaping Yin, Xuejun Deng 2014, 9 (5):  526-533.  doi: 10.4103/1673-5374.130083 Abstract ( 190 )   PDF (2325KB) ( 1159 )   Save Temporal lobe epilepsy is associated with astrogliosis. Notch1 signaling can induce astrogliosis in glioma. However, it remains unknown whether Notch1 signaling is involved in the pathogenesis of epilepsy. This study investigated the presence of Notch1, hairy and enhancer of split-1, and glial fibrillary acidic protein in the temporal neocortex and hippocampus of lithium-pilocarpine-treated rats. The presence of Notch1 and hairy and enhancer of split-1 was also explored in brain tissues of patients with intractable temporal lobe epilepsy. Quantitative electroencephalogram analysis and behavioral observations were used as auxiliary measures. Results revealed that the presence of Notch1, hairy and enhancer of split-1, and glial fibrillary acidic protein were enhanced in status epilepticus and vehicle-treated spontaneous recurrent seizures rats, but remain unchanged in the following groups: control, absence of either status epilepticus or spontaneous recurrent seizures, and zileuton-treated spontaneous recurrent seizures. Compared with patient control cases, the presences of Notch1 and hairy and enhancer of split-1 were upregulated in the temporal neocortex of patients with intractable temporal lobe epilepsy. Therefore, these results suggest that Notch1 signaling may play an important role in the onset of temporal lobe epilepsy via astrogliosis. Furthermore, zileuton may be a potential therapeutic strategy for temporal lobe epilepsy by blocking Notch1 signaling. References | Related Articles | Metrics

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Adaptive and regulatory mechanisms in aged rats with postoperative cognitive dysfunction Yanlin Bi, Shuyun Liu, Xinjuan Yu, Mingshan Wang, Yuelan Wang 2014, 9 (5):  534-539.  doi: 10.4103/1673-5374.130084 Abstract ( 176 )   PDF (674KB) ( 1049 )   Save Inflammation may play a role in postoperative cognitive dysfunction. 5′ Adenosine monophosphate-activated protein kinase, nuclear factor-kappa B, interleukin-1β, and tumor necrosis factor-α are involved in inflammation. Therefore, these inflammatory mediators may be involved in postoperative cognitive dysfunction. Western immunoblot analysis revealed 5′ adenosine monophosphate-activated protein kinase and nuclear factor-kappa B in the hippocampus of aged rats were increased 1–7 days after splenectomy. Moreover, interleukin-1β and tumor necrosis factor-α were upregulated and gradually decreased. Therefore, these inflammatory mediators may participate in the splenectomy model of postoperative cognitive dysfunction in aged rats. References | Related Articles | Metrics

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Preconditioning crush increases the survival rate of motor neurons after spinal root avulsion Lin Li, Yizhi Zuo, Jianwen He 2014, 9 (5):  540-548.  doi: 10.4103/1673-5374.130096 Abstract ( 172 )   PDF (2776KB) ( 642 )   Save In a previous study, heat shock protein 27 was persistently upregulated in ventral motor neurons following nerve root avulsion or crush. Here, we examined whether the upregulation of heat shock protein 27 would increase the survival rate of motor neurons. Rats were divided into two groups: an avulsion-only group (avulsion of the L4 lumbar nerve root only) and a crush-avulsion group (the L4 lumbar nerve root was crushed 1 week prior to the avulsion). Immunofluorescent staining revealed that the survival rate of motor neurons was significantly greater in the crush-avulsion group than in the avulsion-only group, and this difference remained for at least 5 weeks after avulsion. The higher neuronal survival rate may be explained by the upregulation of heat shock protein 27 expression in motor neurons in the crush-avulsion group. Furthermore, preconditioning crush greatly attenuated the expression of nitric oxide synthase in the motor neurons. Our findings indicate that the neuroprotective action of preconditioning crush is mediated through the upregulation of heat shock protein 27 expression and the attenuation of neuronal nitric oxide synthase upregulation following avulsion. References | Related Articles | Metrics

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Analysis of the effect of repeated-pulse transcranial magnetic stimulation at the Guangming point on electroencephalograms Xin Zhang, Lingdi Fu, Yuehua Geng, Xiang Zhai, Yanhua Liu 2014, 9 (5):  549-554.  doi: 10.4103/1673-5374.130082 Abstract ( 176 )   PDF (542KB) ( 1072 )   Save Here, we administered repeated-pulse transcranial magnetic stimulation to healthy people at the left Guangming (GB37) and a mock point, and calculated the sample entropy of electroencephalogram signals using nonlinear dynamics. Additionally, we compared electroencephalogram sample entropy of signals in response to visual stimulation before, during, and after repeated-pulse transcranial magnetic stimulation at the Guangming. Results showed that electroencephalogram sample entropy at left (F3) and right (FP2) frontal electrodes were significantly different depending on where the magnetic stimulation was administered. Additionally, compared with the mock point, electroencephalogram sample entropy was higher after stimulating the Guangming point. When visual stimulation at Guangming was given before repeated-pulse transcranial magnetic stimulation, significant differences in sample entropy were found at five electrodes (C3, Cz, C4, P3, T8) in parietal cortex, the central gyrus, and the right temporal region compared with when it was given after repeated-pulse transcranial magnetic stimulation, indicating that repeated-pulse transcranial magnetic stimulation at Guangming can affect visual function. Analysis of electroencephalogram revealed that when visual stimulation preceded repeated pulse transcranial magnetic stimulation, sample entropy values were higher at the C3, C4, and P3 electrodes and lower at the Cz and T8 electrodes than visual stimulation followed preceded repeated pulse transcranial magnetic stimulation. The findings indicate that repeated-pulse transcranial magnetic stimulation at the Guangming evokes different patterns of electroencephalogram signals than repeated-pulse transcranial magnetic stimulation at other nearby points on the body surface, and that repeated-pulse transcranial magnetic stimulation at the Guangming is associated with changes in the complexity of visually evoked electroencephalogram signals in parietal regions, central gyrus, and temporal regions. References | Related Articles | Metrics

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Acrylamide exposure impairs blood-cerebrospinal fluid barrier function Xue Yao, Licheng Yan, Lin Yao, Weijun Guan, Fanxu Zeng, Fuyuan Cao, Yanshu Zhang 2014, 9 (5):  555-560.  doi: 10.4103/1673-5374.130080 Abstract ( 193 )   PDF (222KB) ( 939 )   Save Previous studies show that chronic acrylamide exposure leads to central and peripheral neuropathy. However, the underlying mechanisms remained unclear. In this study, we examined the permeability of the blood-cerebrospinal fluid barrier, and its ability to secrete transthyretin and transport leptin of rats exposed to acrylamide for 7, 14, 21 or 28 days. Transthyretin levels in cerebrospinal fluid began to decline on day 7 after acrylamide exposure. The sodium fluorescein level in cerebrospinal fluid was increased on day 14 after exposure. Evans blue concentration in cerebrospinal fluid was increased and the cerebrospinal fluid/serum leptin ratio was decreased on days 21 and 28 after exposure. In comparison, the cerebrospinal fluid/serum albumin ratio was increased on day 28 after exposure. Our findings show that acrylamide exposure damages the blood-cerebrospinal fluid barrier and impairs secretory and transport functions. These changes may underlie acrylamide-induced neurotoxicity. Related Articles | Metrics