Evidence of increased brain amyloid in severe TBI survivors at 1, 12, and 24 months after injury: report of 2 cases

Traumatic brain injury (TBI) is a major risk factor for Alzheimer’s disease. With respect to amyloid deposition, there are no published serial data regarding the deposition rate of amyloid throughout the brain after TBI. The authors conducted serial 18F-AV-45 (florbetapir F18) positron emission tomography (PET) imaging in 2 patients with severe TBI at 1, 12, and 24 months after injury. A total of 12 brain regions were surveyed for changes in amyloid levels. Case 1 involved a 50-year-old man who experienced a severe TBI. Compared with the 1-month time point, of the 12 brain regions that were surveyed, a decrease in amyloid (as indicated by standard uptake value ratios) was only observed in the hippocampus (−16%, left; −12%, right) and caudate nucleus (−18%, left; −18%, right), suggesting that initial amyloid accumulation in the brain was cleared between time points 1 and 12 months after injury. Compared to the scan at 1 year, a greater increase in amyloid (+15%) was observed in the right hippocampus at the 24-month time point. The patient in Case 2 was a 37-year-old man who suffered severe trauma to the head and a subsequent stroke; he had poor cognitive/functional outcomes and underwent 1.5 years of rehabilitation. Due to a large infarct area on the injured side of the brain (right side), the authors focused primarily on brain regions affected within the left hemisphere. Compared with the 1-month scan, they only found an increase in brain amyloid within the left anterior putamen (+11%) at 12 months after injury. In contrast, decreased amyloid burden was detected in the left caudate nucleus (−48%), occipital cortex (−21%), and precuneus (−19%) brain regions at the 12-month time point, which is indicative of early accumulation and subsequent clearance. In comparison with 12-month values, more clearance was observed, since a reduction in amyloid was found at 24 months after trauma within the left anterior putamen (−12%) and occipital cortex (−15%). Also, by 24 months, most of the amyloid had been cleared and the patient demonstrated improved results on the Rivermead symptom questionnaire, Glasgow Outcome Scale-Extended, and Disability Rating Scale. With respect to APOE status, the patient in Case 1 had two ε3 alleles and the patient in Case 2 had one ε2 and one ε3 allele. In comparison to the findings of the initial scan at 1 month after TBI, by 12 and 24 months after injury amyloid was cleared in some brain regions and increased in others. Serial imaging conducted here suggests that florbetapir F18 PET imaging may be useful in monitoring amyloid dynamics within specific brain regions following severe TBI and may be predictive of cognitive deficits.

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Potential for imaging the high-affinity state of the 5-HT1B receptor: a comparison of three PET radioligands with differing intrinsic activity

EJNMMI Research ◽

10.1186/s13550-019-0570-1 ◽

2019 ◽

Vol 9 (1) ◽

Author(s):

Anton Lindberg ◽

Ryosuke Arakawa ◽

Tsuyoshi Nogami ◽

Sangram Nag ◽

Magnus Schou ◽

...

Keyword(s):

Pet Imaging ◽

Specific Binding ◽

Occipital Cortex ◽

Intrinsic Activity ◽

High Affinity ◽

G Protein Coupled ◽

Dose Dependent ◽

The Brain ◽

Agonist Affinity States ◽

Different Doses

Abstract Background Over the last decade, a few radioligands have been developed for PET imaging of brain 5-HT1B receptors. The 5-HT1B receptor is a G-protein-coupled receptor (GPCR) that exists in two different agonist affinity states. An agonist ligand is expected to be more sensitive towards competition from another agonist, such as endogenous 5-HT, than an antagonist ligand. It is of interest to know whether the intrinsic activity of a PET radioligand for the 5-HT1B receptor impacts on its ability to detect changes in endogenous synaptic 5-HT density. Three high-affinity 11C-labeled 5-HT1B PET radioligands with differing intrinsic activity were applied to PET measurements in cynomolgus monkey to evaluate their sensitivity to be displaced within the brain by endogenous 5-HT. For these experiments, fenfluramine was pre-administered at two different doses (1.0 and 5.0 mg/kg, i.v.) to induce synaptic 5-HT release. Results A dose-dependent response to fenfluramine was detected for all three radioligands. At the highest dose of fenfluramine (5.0 mg/kg, i.v.), reductions in specific binding in the occipital cortex increased with radioligand agonist efficacy, reaching 61% for [11C]3. The most antagonistic radioligand showed the lowest reduction in specific binding. Conclusions Three 5-HT1B PET radioligands were identified with differing intrinsic activity that could be used in imaging high- and low-affinity states of 5-HT1B receptors using PET. From this limited study, radioligand sensitivity to endogenous 5-HT appears to depend on agonist efficacy. More extensive studies are required to substantiate this suggestion.

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Glutamine synthetase expression in the brain during experimental acute liver failure (immunohistochemical study)

Journal of Education, Health and Sport ◽

10.12775/jehs.2021.11.10.033 ◽

2021 ◽

Vol 11 (10) ◽

pp. 342-356

Author(s):

T. Shulyatnikova ◽

V. Tumanskiy

Keyword(s):

White Matter ◽

Glutamine Synthetase ◽

Liver Failure ◽

Acute Liver Failure ◽

Caudate Nucleus ◽

Immunohistochemical Study ◽

Clinical Signs ◽

Brain Regions ◽

Progressive Increase ◽

The Brain

The aim of the study was to determine the immunohistochemical level of glutamine synthetase (GS) expression in different brain regions in the conditions of experimental acute liver failure in rats. Materials and methods. The study was conducted in Wistar rats: 5 sham (control) animals and 10 rats with acetaminophen induced liver failure model (AILF). The immunohistochemical study of GS expression in the sensorimotor cortex, white matter, hippocampus, thalamus, caudate nucleus/putamen was carried out in the period of 12-24 h after acetaminophen treatment. Results. Beginning from the 6th hour after acetaminophen treatment all AILF-animals showed the progressive increase in clinical signs of acute brain disfunction finished in 6 rats by comatose state up to 24 h - they constituted subgroup AILF-B, “non-survived”. 4 animals survived until the 24 h - subgroup AILF-A, “survived”. In the AILF-B group, starting from 16 to 24 hours after treatment, a significant (relative to control) regionally-specific dynamic increase in the level of GS expression was observed in the brain: in the cortex – by 307.33 %, in the thalamus – by 249.47%, in the hippocampus – by 245.53%, in the subcortical white matter – by 126.08%, from 12th hour – in the caudate nucleus/putamen, by 191.66 %; with the most substantive elevation of GS expression in the cortex: by 4.07 times. Conclusion. Starting from the 16th hours after the acetaminophen treatment (from the 12th h in the caudate nucleus/putamen region) and up to 24 h, it is observed reliable compared to control dynamic increase in GS protein expression in the cortex, white matter, hippocampus, thalamus, caudate nucleus/putamen of the rat brain with the most significant elevation in the cortex among other regions. The heterogeneity in the degree of GS expression rising in different brain regions potentially may indicate regions more permeable for ammonia and/or other systemic toxic factors as well as heterogeneous sensitivity of brain regions to deleterious agents in conditions of AILF. Subsequently, revealed diversity in the GS expression reflects the specificity of reactive response of local astroglia in the condition of AILF-encephalopathy during specific time-period. The dynamic increase in the GS expression associated with impairment of animal state, indicates involvement of increased GS levels in the mechanisms of experimental acute hepatic encephalopathy.

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Connectome Analysis of Brain Functional Network Alterations in Depressive Patients with Suicidal Attempt

Journal of Clinical Medicine ◽

10.3390/jcm8111966 ◽

2019 ◽

Vol 8 (11) ◽

pp. 1966 ◽

Cited By ~ 2

Author(s):

Jun-Cheng Weng ◽

Yu-Syuan Chou ◽

Yuan-Hsiung Tsai ◽

Chun-Te Lee ◽

Ming-Hong Hsieh ◽

...

Keyword(s):

Suicide Attempt ◽

Depressive Disorders ◽

Rating Scale ◽

Suicide Attempts ◽

Imaging System ◽

Brain Regions ◽

Healthy Controls ◽

Depressed Patients ◽

The Brain ◽

Healthy Participants

Our study aimed to clarify the neuroimaging correlates of suicide attempt by comparing differences in functional magnetic resonance imaging (fMRI) among depressed suicide attempters, depressed patients without suicide attempt history, and healthy controls through comprehensive and novel fMRI analyses and methods in the same study population. The association between depression severity and aspects of the brain imaging was also discussed. Our study recruited 109 participants who were assigned to three groups: 33 depressed patients with suicide attempt (SA), 32 depressed patients without suicide attempt (NS), and 44 healthy controls (HC). All participants were scanned using a 3 T MRI imaging system to obtain resting-state functional images. In seed-based correlation analysis, we found altered functional connectivity in some brain regions of the SA compared with the NS or HC, especially in the hippocampus and thalamus. In the voxel-based analysis, our results showed differential activation and regional homogeneity of the temporal lobe and several brain regions in the SA compared with the NS and HC. We also found that some brain areas correlated with the Hamilton Depression Rating Scale (HAM-D), anxiety, and depression scores, especially in the frontal and temporal lobes. Graph theoretical analysis (GTA) and network-based statistical (NBS) analyses revealed different topological organization as well as slightly better global integration and worse local segregation of the brain network (i.e., more like a random network) in depressed participants compared with healthy participants. We concluded that the brain function of major depressive disorders with and without suicide attempts changed compared with healthy participants.

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Reversibility of Neuroimaging Markers Influenced by Lifetime Occupational Manganese Exposure

Toxicological Sciences ◽

10.1093/toxsci/kfz174 ◽

2019 ◽

Vol 172 (1) ◽

pp. 181-190 ◽

Cited By ~ 1

Author(s):

David A Edmondson ◽

Ruoyun E Ma ◽

Chien-Lin Yeh ◽

Eric Ward ◽

Sandy Snyder ◽

...

Keyword(s):

Magnetic Resonance ◽

Rating Scale ◽

Body Burden ◽

Brain Regions ◽

Cumulative Exposure ◽

Resonance Spectroscopy ◽

Manganese Exposure ◽

Disease Rating ◽

Magnetic Resonance Imaging Mri ◽

The Brain

Abstract Manganese (Mn) is a neurotoxicant that many workers are exposed to daily. There is limited knowledge about how changes in exposure levels impact measures in magnetic resonance imaging (MRI). We hypothesized that changes in Mn exposure would be reflected by changes in the MRI relaxation rate R1 and thalamic γ-aminobutyric acid (GABAThal). As part of a prospective cohort study, 17 welders were recruited and imaged on 2 separate occasions approximately 2 years apart. MRI relaxometry was used to assess changes of Mn accumulation in the brain. Additionally, GABA was measured using magnetic resonance spectroscopy in the thalamic and striatal regions of the brain. Air Mn exposure ([Mn]Air) and cumulative exposure indexes of Mn (Mn-CEI) for the past 3 months (Mn-CEI3M), past year (Mn-CEI12M), and lifetime (Mn-CEILife) were calculated using personal air sampling and a comprehensive work history, whereas toenails were collected for analysis of internal Mn body burden. Finally, welders’ motor function was examined using the Unified Parkinson’s Disease Rating Scale (UPDRS). Median exposure decreased for all exposure measures between the first and second scan. ΔGABAThal was significantly correlated with ΔMn-CEI3M (ρ = 0.66, adjusted p = .02), ΔMn-CEI12M (ρ = 0.70, adjusted p = .006), and Δ[Mn]Air (ρ = 0.77, adjusted p = .002). ΔGABAThal significantly decreased linearly with ΔMn-CEI3M (quantile regression, β = 15.22, p = .02) as well as Δ[Mn]Air (β = 1.27, p = .04). Finally, Mn-CEILife interacted with Δ[Mn]Air in the substantia nigra where higher Mn-CEILife lessened the ΔR1 per Δ[Mn]Air (F-test, p = .005). Although R1 and GABA changed with Mn exposure, UPDRS was unaffected. In conclusion, our study shows that effects from changes in Mn exposure are reflected in thalamic GABA levels and brain Mn levels, as measured by R1, in most brain regions.

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Abstract 48: Reduction of Histological Damage with Mild Therapeutic Hypothermia after Prolonged Cardiac Arrest

Circulation ◽

10.1161/circ.116.suppl_16.ii_933-b ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Gregor Springler ◽

Andreas Janata ◽

Wolfgang Weihs ◽

Keywan Bayegan ◽

Alexandra Schratter ◽

...

Keyword(s):

Cardiac Arrest ◽

Occipital Cortex ◽

Brain Regions ◽

Control Group ◽

Surface Cooling ◽

Vacuolar Degeneration ◽

Damage Score ◽

Histological Damage ◽

Hypothermia Group ◽

The Brain

Purpose: The aim of our study was to assess the effect of hypothermia on histological damage in 19 brain regions after prolonged cardiac arrest in pigs. Methods: Pigs were anaesthetized and mechanically ventilated. After stabilisation of pulmonary artery temperature (Tpa) at 38.5±0.2 °C, ventricular fibrillation (VF) was induced and 10 min of untreated VF were followed by 8 min of cardiopulmonary resuscitation (mechanical chest compressions, two doses of vasopressin 0.4 IE/kg). At 8 min of CPR, up to 3 countershocks were delivered. Pigs that had return of spontaneous circulation (ROSC) were randomized to one of 2 groups (control, hypothermia). Pigs in the hypothermia group were cooled to Tpa 33.0±1.0 °C with a surface cooling device (LRS Thermosuit™) circulating ice water over most of the skin surface. Pigs in the control group were kept at 38.5±1.0 °C throughout the experiment. After 14 hours of hypothermia, pigs were rewarmed, weaned and brought to the stable. At day 9 of the experiment, final neurologic examination was performed. After that the animals were sacrificed and perfused with 4 liters of saline, followed by 1 liter of paraformaldehyde (3%, pH 7.4). The brain was removed and 19 different regions of the brain were examined by means of lightmicroscopy using a histopathologic damage score that was used in previous studies. Following damage qualities were considered: edema, eosinophilic necrosis (oncosis), vacuolar degeneration and malacia. The total numeric histological damage score (HDS) was the sum of all area scores. Data are presented as median and interquartile range, group comparison was done with a Mann-Whitney-U test. Results: 16 (29 –35 kg) pigs were randomized. The time to reach target temperature in the hypothermia group (n = 8) was 9.0 (5.3; 11.9) min. Total HDS in the hypothermia group was 71 (61; 84), in the control group 132 (124; 174; p<0.001). Significant (p<0.05) improvements in damage were found in hippocampus, temporal, parietal, frontal and occipital cortex. Conclusions: Histological damage after prolonged cardiac arrest was improved significantly in cooled animals compared to control animals. Not all brain regions could benefit to the same extent.

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Neural underpinnings of morality judgment and moral aesthetic judgment

Scientific Reports ◽

10.1038/s41598-021-97782-7 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Qiuping Cheng ◽

Xue Wen ◽

Guozhen Ye ◽

Yanchi Liu ◽

Yilong Kong ◽

...

Keyword(s):

Brain Activity ◽

Temporal Cortex ◽

Occipital Cortex ◽

Brain Regions ◽

Aesthetic Judgment ◽

Aesthetic Pleasure ◽

Neural Underpinnings ◽

Motor Representations ◽

The Relationship ◽

The Brain

AbstractMorality judgment usually refers to the evaluation of moral behavior`s ability to affect others` interests and welfare, while moral aesthetic judgment often implies the appraisal of moral behavior's capability to provide aesthetic pleasure. Both are based on the behavioral understanding. To our knowledge, no study has directly compared the brain activity of these two types of judgments. The present study recorded and analyzed brain activity involved in the morality and moral aesthetic judgments to reveal whether these two types of judgments differ in their neural underpinnings. Results reveled that morality judgment activated the frontal, parietal and occipital cortex previously reported for motor representations of behavior. Evaluation of goodness and badness showed similar patterns of activation in these brain regions. In contrast, moral aesthetic judgment elicited specific activations in the frontal, parietal and temporal cortex proved to be involved in the behavioral intentions and emotions. Evaluation of beauty and ugliness showed similar patterns of activation in these brain regions. Our findings indicate that morality judgment and moral aesthetic judgment recruit different cortical networks that might decode others' behaviors at different levels. These results contribute to further understanding of the essence of the relationship between morality judgment and aesthetic judgment.

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Immunohistochemical analysis of GFAP expression in the experimental sepsis-associated encephalopathy

Pathologia ◽

10.14739/2310-1237.2021.3.240033 ◽

2021 ◽

Vol 18 (3) ◽

pp. 295-302

Author(s):

T. V. Shulyatnikova ◽

V. O. Tumaskyi

Keyword(s):

White Matter ◽

Caudate Nucleus ◽

Critical Role ◽

Brain Regions ◽

Subcortical White Matter ◽

Control Group ◽

Experimental Sepsis ◽

Respiratory Impairment ◽

Gfap Expression ◽

The Brain

Pathophysiology of sepsis-associated encephalopathy (SAE) is linked to blood-brain barrier breakdown, neuroinflammation and neurotransmitter imbalance in the brain. Astroglia, the most abundant cell population within the brain, plays the critical role in control of all kinds of homeostatic processes, thereby regulating the adaptive reactions of the brain to various challenges. Astroglia are highly heterogenous across the brain regions, therefore, damaging factors stimulate heterogenous astroglial reactivity and response in different brain regions. The aim of this study was determining immunohistochemical features of GFAP expression in various brain regions in the model of rodent experimental sepsis. Materials and methods. The experiment was performed in Wistar rats: control group of 5 sham-operated rats and the main group of 20 rats subjected to cecum ligation and puncture (CLP) procedure. The immunohistochemical study of GFAP expression in the sensorimotor cortex, subcortical white matter, hippocampal, thalamic and caudate nucleus/putamen regions was performed from 20 to 48 hours of the postoperative period. Results. Starting from the 12th hour after CLP, animals began display progressive increase in signs of periorbital exudation, piloerection, fever-/hypothermia, diarrhea, social isolation, lethargy, and respiratory impairment. In the period of 20–38 hours, 9 animals showed expressed previously listed symptoms and were euthanized (CLP-B – lethal group), 11 rats survived until 48 hours of the experiment (CLP-A – survived group). In the lethal group, starting from 20 to 38 hours after the CLP procedure, a significant (relative to control) regionally-specific dynamic increase in the level of GFAP expression was observed in the brain: in the cortex – by 465 %, in the subcortical white matter – by 198 %, in the hippocampus – by 250 %, from the 23rd hour – in the caudate nucleus/putamen by 18 %. In the thalamus, no significant changes in the level of GFAP expression were observed. In the cortex and hippocampus of survived animals, 48 h after CLP, higher values of GFAP expression were observed comparing to the group of non-survived animals. Conclusions. Under conditions of the experimental SAE, an early dynamic increase in the astroglial reactivity was observed in the cortex, hippocampus, white matter, and caudate nucleus/putamen of the brain with the most significant increase of indicators in the cortex and hippocampus, which potentially indicates relatively more vulnerable areas of the brain to damaging factors, as well as places of the most active intercellular interaction in the condition of systemic inflammation. Higher values of GFAP expression in the cortex and hippocampus of survived animals at 48 hours of the experiment, compared with indicators of non-survived group, indicate increased astroglial reactivity in these brain regions at the noted time period, accompanied by relatively more favorable clinical course of the disease.

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Dichlorvos Induced AChE Inhibition in Discrete Brain Regions and the Neuro-Cognitive Implications: Ameliorative Effect of Nigella Sativa

Iranian Jornal of Toxicology ◽

10.32598/ijt.12.5.451.2 ◽

2018 ◽

Vol 12 (5) ◽

pp. 11-16

Author(s):

Aminu Imam ◽

◽

Muhammed Adebayo ◽

Wahab Imam Abdulmajeed ◽

Abdulmusawir Alli-Oluwafuyi ◽

...

Keyword(s):

Escape Latency ◽

Nigella Sativa ◽

Occipital Cortex ◽

Brain Regions ◽

Accidental Poisoning ◽

Ache Inhibition ◽

Nissl Staining ◽

Group I ◽

Ameliorative Effect ◽

The Brain

Background: There has been a rise in accidental poisoning cases resulting from the indiscriminate use and exposure to Dichlorvos (DDVP), especially in developing countries, and no antidote with satisfactory efficacy is currently available. Thus, we investigated the AChE reactivation potential of Nigella sativa oil (NSO) following DDVP induced AChE inhibition patterns in the brain and the associated cognitive implications. Methods: Fourty Wistar rats were randomly divided into four groups of 10 each.; The controls were administered PBS (1 ml/kg); DDVP (8.8 mg/kg) was given to the experimental group I; while DDVP+NSO (8.8 mg/kg + 1 ml/kg) and NSO (1 ml/kg) was administered orally to the experimental groups II and III respectively. All treatments lasted for 14 consecutive days. Morris Water Maze (MWM) paradigm was used to assess the working memory, then rats were euthanized, the brain excised, three brains were fixed for histological examination (Nissl staining), and the other seven brains were homogenized for AChE activity and Ca2+ concentrations. Data were analyzed statistically, using ANOVA method and P values of ≤0.05 was considered as significant. Results: In this study, DDVP differentially inhibited AChE activities in various brain regions: cerebellum (86.1%), hippocampus (40.6%), frontal cortex (33.2%), medulla (21.5%), spinal cord (14.8%), and occipital cortex (8.9%). It reduced Ca2+ concentration, but had no effect on the delayed escape latency in the MWM, nor impaired the neuro-architectures. NSO caused increased AChE activities, Ca2+ concentration and reduced escape latency, and improved histologic architectures. Conclusion: We concluded that NSO reactivated DDVP-induced AChE inhibition and improved memory indices, thus, it may serve as a potential treatment in the management of DDVP poisoning cases.

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Neural Underpinnings of Morality Judgment and Moral Aesthetic Judgment

10.21203/rs.3.rs-484056/v1 ◽

2021 ◽

Author(s):

Qiuping Cheng ◽

Xue Wen ◽

Yanchi Liu ◽

Lei Mo

Keyword(s):

Brain Activity ◽

Temporal Cortex ◽

Occipital Cortex ◽

Brain Regions ◽

Aesthetic Judgment ◽

Aesthetic Pleasure ◽

Neural Underpinnings ◽

Motor Representations ◽

The Relationship ◽

The Brain

Abstract Morality judgment usually refers to the evaluation of moral behavior`s ability to affect others` interests and welfare, while moral aesthetic judgment often implies the appraisal of moral behavior's capability to provide aesthetic pleasure. Both are based on the behavioral understanding. To our knowledge, no study has directly compared the brain activity of these two types of judgments. The present study recorded and analyzed brain activity involved in the morality and moral aesthetic judgments to reveal whether these two types of judgments differ in their neural underpinnings. Results reveled that morality judgment activated the frontal, parietal and occipital cortex previously reported for motor representations of behavior. Evaluation of goodness and badness showed similar patterns of activation in these brain regions. In contrast, moral aesthetic judgment elicited specific activations in the frontal, parietal and temporal cortex proved to be involved in the behavioral intentions and emotions. Evaluation of beauty and ugliness showed similar patterns of activation in these brain regions. Our findings indicate that morality judgment and moral aesthetic judgment recruit different cortical networks that might decode others' behaviors at different levels. These results contribute to further understanding of the essence of the relationship between morality judgment and aesthetic judgment.

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Association study of GFAP Polymorphisms with schizophrenia in Han Chinese population

10.21203/rs.2.21670/v1 ◽

2020 ◽

Author(s):

Wenjuan Yu ◽

sidi he ◽

Yimin Yu ◽

Shen He ◽

Qingqing Xu ◽

...

Keyword(s):

Occipital Cortex ◽

Brain Regions ◽

Han Chinese ◽

Eqtl Analysis ◽

Nucleotide Polymorphisms ◽

Han Population ◽

Gfap Expression ◽

Healthy Control ◽

And Control ◽

The Brain

Abstract INTRODUCTION Glial fibrillary acidic protein (GFAP) is considered to be an astrocyte activation marker. Alterations in structural and functional molecules expressed by astrocytes may play a role in the pathophysiology of schizophrenia (SCZ). In the present study, the single nucleotide polymorphisms (SNPs) of GFAP were analyzed for association with schizophrenia in Han population. METHODS Three tag SNPs within GFAP were genotyped in 629 SCZ patients and 655 healthy controls in the Han Chinese population.The schizophrenia database(SCZB) was used to investigate whether GFAP is differentially expressed in the brain regions of schizophrenia and healthy control individuals.In addition, expression quantitative trait loci(eQTL) analysis was used to investigate differential GFAP expression between different genotypes. RESULTSIt was shown that the rs3785891 GFAP polymorphism may be associated with schizophrenia ( p =0.04). There were no significant differences in the expression of hippocampal, prefrontal cortex or cortical GFAP between schizophrenia patients and control individuals. Furthermore,the brain eQTL analysis revealed a significant association between the rs3785891 polymorphism and GFAP expression in the intralobular white matter ( p = 0.04), thalamus ( p =0.024), hippocampus ( p =0.011), and occipital cortex ( p =0.0075). CONCLUSIONS This study shows that rs3785891 may be linked to schizophrenia susceptibility in the Han population. Further study is required for clarification the role of genetic variation around these SNPs in expression pattern of the GFAP gene, which may be involved in schizophrenia pathogenesis.

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