Neuropsychological, plasma marker, and functional connectivity changes in Alzheimer's disease patients infected with COVID-19.

Introduction: Patients with COVID-19 may experience various neurological conditions, including cognitive impairment, encephalitis, and stroke. This is particularly significant in individuals who already have Alzheimer's disease (AD), as the cognitive impairments can be more pronounced in these cases. However, the extent and underlying mechanisms of cognitive impairments in COVID-19-infected AD patients have yet to be fully investigated through clinical and neurophysiological approaches. Methods: This study included a total of 77 AD patients. Cognitive functions were assessed using neuropsychiatric scales for all participants, and plasma biomarkers of amyloid protein and tau protein were measured in a subset of 25 participants. To investigate the changes in functional brain connectivity induced by COVID-19 infection, a cross-sectional neuroimaging design was conducted involving a subset of 37 AD patients, including a control group of 18 AD participants without COVID-19 infection and a COVID-19 group consisting of 19 AD participants. Results: For the 77 AD patients between the stages of pre and post COVID-19 infection, there were significant differences in cognitive function and psychobehavioral symptoms on the Montreal Scale (MoCA), the neuropsychiatric inventory (NPI), the clinician's global impression of change (CIBIC-Plus), and the activity of daily living scale (ADL). The COVID-19 infection significantly decreased the plasma biomarker level of Aß42 and increased the plasma p-tau181 level in AD patients. The COVID-19-infected AD patients show decreased local coherence (LCOR) in the anterior middle temporal gyrus and decreased global correlation (GCOR) in the precuneus and the medial prefrontal cortex. Conclusion: The findings suggest clinical, cognitive, and neural alterations following COVID-19 infection in AD patients and emphasize the need for close monitoring of symptoms in AD patients who have had COVID-19 and further exploration of the underlying mechanisms.

Analysis on the Risk Factors of Malnutrition in Type 2 Diabetes Mellitus Patients with Pulmonary Tuberculosis.

Objective: To explore the risk factors of malnutrition in type 2 diabetes mellitus combined with pulmonary tuberculosis (PTB-T2DM) patients and further to provide a clinical research basis for the identification and prevention of malnutrition. Methods: From January 2020 to February 2022, 307 adult patients diagnosed with PTB-T2DM were enrolled in this retrospective study. According to whether malnutrition occurred after 6 months of treatment, patients were divided into malnutrition group (n = 123) and non-malnutrition group (n = 184). The nutritional status of patients was evaluated according to the Micro-Nutrition Assessment Scale (MNA). Evaluation of indicators was performed, including general information, disease characteristics of PTB-T2DM and laboratory indicators. Results: Univariate logistic regression analysis showed that drinking, divorced, BMI <18.5kg/m2, weight <45kg, waist circumference <79cm, hip circumference <88cm, waist-to-hip ratio <69.99, calf circumference <26kg, grip strength <28kg, NRS score ≥3, Hb <106g/L, Alb <29.00g/L, PA <48.00µmol/L, GHB <3.40%, serum transferrin <1.37 mmol/L, serum potassium <3.18mmol/L, serum sodium <142.95 mmol/L, FEV1 ≥67.90% and RV <2.89% were risk factors for malnutrition in PTB-T2DM patients (all P < 0.05). The results of multivariate logistic regression analysis showed that drinking, divorced, weight <45kg, BMI <18.5kg/m2, NRS score ≥3, Hb <106g/L, Alb <29.00g/L, PA <48.00µmol/L, serum transferrin <1.37mmol/L, FEV1 ≥67.90% and RV <2.89% were independent risk factors for malnutrition in PTB-T2DM patients (all P < 0.05). Conclusion: Drinking, divorced, weight <45kg, BMI <18.5kg/m2, NRS score ≥3, Hb <106g/L, Alb <29.00g/L, PA <48.00µmol/L, serum transferrin <1.37mmol/L, FEV1 ≥67.90% and RV <2.89% may be independent risk factors for malnutrition in PTB-T2DM patients, and timely identification of high-risk groups could improve the prognosis of PTB-T2DM patients.

Analysis of Clinical Characteristics and Risk Factors for Drug Resistance in Newly-Treated Patients with Pulmonary Tuberculosis Complicated with Chronic Obstructive Pulmonary Disease.

Objective: To analyze the clinical characteristics and risk factors of drug resistance of newly-treated chronic obstructive pulmonary disease (COPD) complicated pulmonary tuberculosis (PTB). Methods: A total of 489 newly-treated PTB patients admitted to Beijing Geriatric hospital were retrospectively enrolled in this study. Of these, 138 patients with COPD were allocated to the study group, and the remaining 351 patients without COPD were allocated to the control group. The baseline information, clinical characteristics of PTB and drug resistance of Mycobacterium tuberculosis were compared between the two groups. Logistic regression was used to explore the correlation between drug resistance and COPD complications. Results: Patients complicated with COPD had a higher proportion of respiratory failure, cough, fever and night sweats, chest short breath, and emaciation between the study group and the control group (P<0.05). In terms of medical history, patients complicated with COPD also had a higher proportion of childhood TB history, cough, tuberculosis exposure rate, dust exposure rate, and malnutrition (P<0.05). There were significantly more patients with pulmonary cavities and a delayed diagnosis of TB in the study group than in the control group (P<0.05). The single drug resistance rates of isoniazid, ethambutol, rifampicin, pyrazinamide, and rifapentine, and drug resistance with any two or more drugs in the study group were significantly higher than those in the control group (P<0.05). Multivariate Logistic regression analysis showed that smoking, extrapulmonary tuberculosis, tuberculosis exposure history, malnutrition, pulmonary cavity, and delayed TB diagnosis were risk factors for drug resistance in newly-treated COPD complicated PTB patients. Conclusion: The symptoms of COPD complicated PTB were more serious. Smoking history, extrapulmonary tuberculosis, tuberculosis exposure history, malnutrition, pulmonary cavity, and delayed diagnosis of tuberculosis were risk factors for TB resistance in these patients.

Relationship Between Alzheimer's Disease and Retinal Choroidal Thickness: A Cross-Sectional Study.

BACKGROUND: The choroid is involved directly or indirectly in many pathological conditions such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). OBJECTIVE: The objective of this study was to investigate the association between retinal choroidal properties and the pathology of AD by determining choroidal thickness, hippocampus volume, cognitive functions, and plasma BACE1 activity. METHODS: In this cross-sectional study, 37 patients with AD and 34 age-matched controls were included. Retinal choroidal thickness was measured via enhanced depth imaging optical coherence tomography. Hippocampal volume was measured via 3.0T MRI. Cognitive functions were evaluated using the Mini-Mental State Examination (MMSE) and Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-Cog). Plasma BACE1 activity was analyzed using a fluorescence substrate-based plasma assay, and regression model were to analyze the data. RESULTS: Retinal choroidal thickness was significantly thinner in the AD group than in the control group [(114.81±81.30) µm versus (233.79±38.29) µm, p < 0.05]. Multivariable regression analysis indicated that the ADAS-cog scores (ß=-0.772, p = 0.000) and age (ß=-0.176, p = 0.015) were independently associated with choroidal thickness. The logistic regression model revealed that the subfoveal choroidal thickness was a significant predictor for AD (OR = 0.984, 95% CI: 0.972-0.997). CONCLUSION: There was a general tendency of choroid thinning as the cognitive function declined. Although choroidal thickness was not a potential indicator for early stage AD, it was valuable in monitoring AD progression.

Safety and Efficacy of 630-nm Red Light on Cognitive Function in Older Adults With Mild to Moderate Alzheimer's Disease: Protocol for a Randomized Controlled Study.

Introduction: Studies have shown that excess formaldehyde accumulation in the brain accelerates cognitive decline in people with Alzheimer's disease (AD). Recently, reports from our research team revealed that red light treatment (RLT) improved memory in AD mice by activating formaldehyde dehydrogenase (FDH) and thus reducing formaldehyde levels. Here, we developed a medical RLT device to investigate the safety and efficacy of this device in older adults with mild to moderate AD. Methods: This will be a randomized controlled trial (RCT) that will include 60 participants who will be recruited and randomly divided into an RLT group and a control group. The RLT group will receive RLT intervention 5 days a week for 30 min each time for 24 weeks while the control group will continue their routine treatments without RLT. All participants will undergo neuropsychological and functional assessments including the Mini-Mental State Examination, the AD assessment scale-cognitive subscale (ADAS-cog), the Geriatric Depression Scale (GDS), the Neuropsychiatric Inventory (NPI) and the Barthel Index at baseline, 12 weeks and 24 weeks. All participants will undergo functional magnetic resonance imaging (fMRI) scanning and blood/urine biomarkers tests at baseline and 24 weeks. The primary outcome will be the ADAS-cog score while the secondary outcomes will be the GDS and NPI scores. Adverse events will be recorded and treated when necessary. Both an intention-to-treat analysis and a per-protocol analysis will be performed to evaluate the safety and efficacy of RLT. Discussion: This protocol outlines the objectives of the study and explained the RLT device developed by the research team. The study is designed as an RCT to evaluate the safety and effects of the RLT device on older adults with mild to moderate AD. This study will provide evidence for the clinical use of RLT on treatment for AD. Clinical Trial Registration: www.ClinicalTrials.gov, ChiCTR1800020163; Pre-results.

Efficacy of Group Reminiscence Therapy on Cognition, Depression, Neuropsychiatric Symptoms, and Activities of Daily Living for Patients With Alzheimer Disease.

The current study aimed to investigate the effects of group reminiscence therapy on cognitive function, depression, neuropsychiatric symptoms, and activities of daily living in patients with mild-to-moderate Alzheimer disease (AD). A single-blind randomized parallel-design controlled trial was conducted between May 1, 2017, and April 30, 2018. Ninety patients with mild-to-moderate AD recruited from Beijing Geriatric Hospital were randomly allocated into intervention (n = 45) and control groups (n = 45). In the intervention group, group-based reminiscence therapy was performed in two 30- to 45-minute sessions weekly for 12 weeks. Control participants received only conventional drug treatments and routine daily care. Alzheimer disease-related symptoms were evaluated using the Alzheimer's Disease Assessment Scale-Cognitive section, the Cornell Scale for Depression in Dementia (CSDD), the Neuropsychiatric Inventory, and the Barthel Index. Four time points were set for data collection: baseline (before treatment), 4 weeks (during treatment), 12 weeks (end of treatment), and 24 weeks (12 weeks posttreatment). χ2 Tests, independent t tests, repeated-measures analysis of variance, and Bonferroni tests were used for data analysis. Significant improvements in depressive and neuropsychiatric symptoms were found in the intervention group compared to the control group (P < .05). Mean CSDD scores in the intervention group were improved at all 3 time points compared to baseline and showed the greatest effect at 12 weeks (t = 2.076, P = .041) and 24 weeks follow-up (t = 3.834, P = .000) compared to controls. Group reminiscence therapy was effective for improving depressive symptoms and was beneficial for treating neuropsychiatric symptoms in patients with AD.

Interferon-γ Potentiates α-Synuclein-induced Neurotoxicity Linked to Toll-like Receptors 2 and 3 and Tumor Necrosis Factor-α in Murine Astrocytes.

α-Synuclein (α-syn), a metabolite of neurons, induces glial activation and neuroinflammation and participates in pathogenesis of neurodegenerative diseases. This inflammatory response involves activation of toll-like receptors (TLRs) and its neurotoxic outcomes such as cytokine expression and release. However, regulatory role of cytokines on α-syn-induced neurotoxicity is still unclear. In this study, we used interferon (IFN)-γ to costimulate primary astrocytes with wild-type or A53T mutant α-syn, and evaluated inflammatory pathway activation. Four α-syn concentrations (0.5, 2, 8 and 20 µg/mL, 24 h) and four α-syn time-points (3, 12, 24 and 48 h, 2 µg/mL) were chosen to coincubate with one IFN-γ concentration (2 ng/mL). IFN-γ alone upregulated expressions of TLR3 and tumor necrosis factor (TNF)-α (mRNA level), and A53T mutant or wild-type α-syn alone activated the pathway components including TLR2, TLR3, nuclear factor-κB, TNF-α and interleukin (IL)-1ß. Additive application of IFN-γ amplified this activation effect except for IL-1ß at mRNA and protein levels or TNF-α release, displaying a synergistic effect of α-syn and IFN-γ. Blocking TLR2 other than TLR4 suppressed TLR3, TLR2 and TNF-α expressions induced by α-syn or plus IFN-γ, reflecting an interaction of TLR2 and TLR3 in TNF-α expression. These data collectively showed that IFN-γ potentiated α-syn stimulation and inflammatory outcomes via TLR2, TLR3 and TNF-α other than IL-1ß in astrocytes, suggesting that involvement of IFN-γ in α-syn-induced innate immunity may be required for initiation and maintenance of glial activation, a novel neurotoxic mechanism underlying pathogenesis of neurodegenerative diseases. Graphical Abstract IFN-γ potentiates α-synuclein (A53T or wild-type)-induced innate immunity, involving expressions of TLR2, TLR3, NF-κB, and TNF-α, other than IL-1ß. This effect is suppressed by blockage of TLR2 other than TLR4, reflecting an interaction of TLR2 and TLR3 in TNF-α expression. Thus, involvement of IFN-γ in α-syn-induced neurotoxicity may be required for initiation and maintenance of glial activation, a novel neurotoxic mechanism underlying pathogenesis of neurodegenerative diseases.

The Effects of Music Therapy on Cognition, Psychiatric Symptoms, and Activities of Daily Living in Patients with Alzheimer's Disease.

BACKGROUND: Alzheimer's disease (AD) is the most common type of dementia, affecting millions of older people worldwide. However, pharmacological therapies have not achieved desirable clinical efficacy in the past decades. Non-pharmacological therapies have been receiving increased attention to treat dementia in recent years. OBJECTIVE: This study explores the effects of music therapy on cognitive function and mental wellbeing of patients with AD. METHODS: A total number of 298 AD patients with mild, moderate, or severe dementia participated in the study. The participants with each grade of severity were randomly divided into three groups, which were a singing group, a lyric reading group, and a control group. These three groups received different interventions for three months. All participants underwent a series of tests on cognitive functions, neuropsychological symptoms, and activities of daily living at baseline, three months, and six months. RESULTS: The analysis shows that music therapy is more effective for improving verbal fluency and for alleviating the psychiatric symptoms and caregiver distress than lyrics reading in patients with AD. Stratified analysis shows that music therapy is effective for enhancing memory and language ability in patients with mild AD and reducing the psychiatric symptoms and caregiver distress in patients with moderate or severe AD. However, no significant effect was found for activities of daily living in patients with mild, moderate, or severe AD. CONCLUSION: This study suggests that music therapy is effective in enhancing cognitive function and mental wellbeing and can be recommended as an alternative approach to manage AD associated symptoms.

α-Synuclein activates innate immunity but suppresses interferon-γ expression in murine astrocytes.

Glial activation and neuroinflammation contribute to pathogenesis of neurodegenerative diseases, linked to neuron loss and dysfunction. α-Synuclein (α-syn), as a metabolite of neuron, can induce microglia activation to trigger innate immune response. However, whether α-syn, as well as its mutants (A53T, A30P, and E46K), induces astrocyte activation and inflammatory response is not fully elucidated. In this study, we used A53T mutant and wild-type α-syns to stimulate primary astrocytes in dose- and time-dependent manners (0.5, 2, 8, and 20 µg/ml for 24 hr or 3, 12, 24, and 48 hr at 2 µg/ml), and evaluated activation of several canonical inflammatory pathway components. The results showed that A53T mutant or wild-type α-syn significantly upregulated mRNA expression of toll-like receptor (TLR)2, TLR3, nuclear factor-κB and interleukin (IL)-1ß, displaying a pattern of positive dose-effect correlation or negative time-effect correlation. Such upregulation was confirmed at protein levels of TLR2 (at 20 µg/ml), TLR3 (at most doses), and IL-1ß (at 3 hr) by western blotting. Blockage of TLR2 other than TLR4 inhibited TLR3 and IL-1ß mRNA expressions. By contrast, interferon (IFN)-γ was significantly downregulated at mRNA, protein, and protein release levels, especially at high concentrations of α-syns or early time-points. These findings indicate that α-syn was a TLRs-mediated immunogenic agent (A53T mutant stronger than wild-type α-syn). The stimulation patterns suggest that persistent release and accumulation of α-syn is required for the maintenance of innate immunity activation, and IFN-γ expression inhibition by α-syn suggests a novel immune molecule interaction mechanism underlying pathogenesis of neurodegenerative diseases.

[Analysis of factors affecting the prognosis of ICU patients by multiple logistic regression model: a retrospective cohort study of 1 299 patients in 12 consecutive years].

OBJECTIVE: To explore the prognostic factors of intensive care unit (ICU) patients. METHODS: A retrospective cohort study was conducted. The clinical data of patients admitted to ICU of Beijing Geriatric Hospital from January 2005 to December 2016 were collected. According to the prognosis, the patients were divided into death group and survival group, and the mortality trend with time and age was observed. Survival and death were treated as dependent variables, while the gender, age, reason of ICU admission, acute physiology and chronic health evaluation II (APACHE II) score, whether undergoing invasive mechanical ventilation (MV), invasive MV reason, duration of invasive MV, whether successful weaning, whether ICU nosocomial infection, hospital acquired pneumonia (HAP), central line-associated bloodstream infection (CLABSI), acute kidney injury (AKI) occurred, whether undergoing continuous blood purification (CBP), whether septic shock occurred, whether undergoing invasive hemodynamic monitoring or blood transfusion and length of ICU stay were used as the independent variables. First, the clinical data was analyzed by univariate analysis. Second, the independent variables influencing the dependent variable were analyzed by logistic regression analysis to screen out prognostic factors of ICU patients. RESULTS: During the study period, 1 325 patients were treated, 26 patients with missing data, 1 299 patients in final group, 865 patients in survival group, and 434 in death group. The proportion of men in the patients was larger (67.7%), and the age span was larger (16-105 years old). The mortality rate in different years showed no significant difference (χ 2 = 16.712, P = 0.117), and with the increase of age, the mortality rate of ICU showed an upward trend (χ 2 = 16.399, P = 0.022). The univariate analysis showed that ICU deaths were unrelated to gender, but associated with age, APACHE II score, invasive MV, invasive MV reason, duration of invasive MV, successful weaning, ICU nosocomial infection, HAP, CLABSI, AKI, septic shock, whether CBP or invasive hemodynamic monitoring, blood transfusion, the reason of ICU admission and the length of ICU stay (all P < 0.05). The relevant factors with statistical difference found in univariate analysis were analyzed in logistic regression analysis, which showed that whether successful weaning [odds ratio (OR) = 0.016, 95% confidence interval (95%CI) = 0.010-0.025], and whether AKI (OR = 3.917, 95%CI = 2.331-6.582) or septic shock occurred (OR = 2.808, 95%CI = 1.604-4.915) were the dependent variables of death or survival (all P = 0.000). Regression coefficient (ß value) of successful weaning was -4.155, suggesting that unsuccessful weaning patients were likely to die. The ß value of AKI and septic shock was 1.365 and 1.033, suggesting that the patients with AKI or septic shock were more likely to die. CONCLUSIONS: Whether the success of weaning, whether the occurrence of AKI or septic shock are independent prognostic factors for the prognosis of ICU patients. Measures for the prevention of the above three aspects could improve the prognosis of ICU patients.

The clinical efficacy of reminiscence therapy in patients with mild-to-moderate Alzheimer disease: Study protocol for a randomized parallel-design controlled trial.

INTRODUCTION: Alzheimer disease (AD) is one of the most common diseases among the older adults. Currently, various nonpharmacological interventions are used for the treatment of AD. Such as reminiscence therapy is being widely used in Western countries. However, it is often used as an empirical application in China; the evidence-based efficacy of reminiscence therapy in AD patients remains to be determined. Therefore, the aim of this research is to assess the effectives of reminiscence therapy for Chinese elderly. METHODS AND ANALYSIS: This is a randomized parallel-design controlled trial. Mild and moderate AD patients who are in the Beijing Geriatric Hospital, China will be randomized into control and intervention groups (n = 45 for each group). For the intervention group, along with conventional drug therapy, participants will be exposed to a reminiscence therapy of 35 to 45 minutes, 2 times/wk for 12 consecutive weeks. Patients in the control group will undergo conventional drug therapy only. The primary outcome measure will be the differences in Alzheimer disease Assessment Scale-Cognitive Section Score. The secondary outcome measures will be the differences in the Cornell scale for depression in dementia, Neuropsychiatric Inventory score, and Barthel Index scores at baseline, at 4 and 12 weeks of treatment, and 12 weeks after treatment. ETHICS AND DISSEMINATION: The protocols have been approved by the ethics committee of Beijing Geriatric Hospital of China (approval no. 2015-010). Findings will be disseminated through presentation at scientific conferences and in academic journals. TRIAL REGISTRATION: Chinese Clinical Trial Registry identifier ChiCTR-INR-16009505.

Neuroprotective Effect of Several Phytochemicals and Its Potential Application in the Prevention of Neurodegenerative Diseases.

The detrimental effects of oxidative stress and chronic neuroinflammation on neuronal cell death have been implicated in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD). The nutritional neuroscience is quickly growing, and phytochemicals or phytobioactive compounds such as curcumin, resveratrol, propolis, ginsenoside, and ω-3 polyunsaturated fatty acids (PUFAs) have been extensively applied to potential therapeutic purposes for numerous neurodegenerative diseases for their anti-oxidative and anti-inflammatory effects. However, their administration as food supplements in the daily diet of the elderly is normally a voluntary and less-organized behavior, indicating the uncertainty of therapeutic effects in this sporadic population; specifically, the effective physiological dosages and the real positive effects in preserving brain health have not yet been fully elucidated. In this review, we collect several lines of evidence on these compounds, which constitute a major type of nutraceuticals and are widely integrated into the daily anti-aging caring of elderly patients, and discuss the underlying anti-oxidative and anti-inflammatory mechanisms of these phytochemicals. In conclusion, we highlight the implications of these compounds in the prevention and treatment of geriatric diseases, and of the potential supplementation procedures used as a dietary therapeutic program in clinical nursing services for patients with neurodegenerative diseases or for the elderly in certain communities, which we hope will lead to more beneficial health outcomes with respect to brain function, innate immunity, and gastrointestinal function, as well as more economic and social benefits.

Cyclin D1 G870A polymorphism and breast cancer risk: a meta-analysis involving 23,998 subjects.

Cyclin D1 (CCND1) plays an essential role in tumor development and progression through regulating the cell transition from G1 to the proliferative S phase. The CCND1 G870A polymorphism has been associated with an increased susceptibility to squamous cell carcinoma of the head and neck, bladder, prostate, and gastric cardiac cancers. There are a number of studies that explored the relationship between CCND1 G870A polymorphism and breast cancer risk, with inconsistent conclusions. In order to better define the predictive value of CCND1 G870A polymorphism in breast cancer, we searched PubMed and EBSCO for relevant publications. A total of 13 studies were indentified, which included 11,235 cases and 12,763 controls. We calculated the summary odds ratios and the corresponding 95% confidence interval. Our meta-analysis showed that carriers of AA genotype have a significantly higher risk in developing breast cancer compared with that of GG genotype (OR = 1.08, 95% CI = 1.01-1.17, p > = 0.03) in overall population. Furthermore, in subgroup analysis, CCND1 G870A polymorphism was associated with a marginally increased risk of breast cancer for Chinese compared to Caucasian populations with an OR = 1.14, 95% CI = 1.00-1.20, p-trend = 0.06 for AA + GA versus GG, if the controls were hospital-based population with an OR = 1.21, 95% CI = 0.99-1.47, p = 0.06 for AA versus GG and if the distributions of genotypes in control groups were consistent with the Hardy-Weinberg equilibrium (HWE) with an OR = 1.08, 95% CI = 1.00-1.15, p = 0.04 for AA versus GA + GG. Our meta-analysis represents the largest study to date indicating that the G870A polymorphism in CCND1 confers an increased risk for breast cancer. Further studies are warranted to explore the preventive measures to detect and manage the breast cancers attributable to the G870A polymorphism.

[Change of neurocytes in acute intoxicated encephalopathy induced by 1, 2-dichloroethane after intervention with antagonists].

OBJECTIVE: To study the role of N-methyl-D-aspartate receptor and Ca(2+) in acute intoxicated encephalopathy induced by 1, 2-dichloroethane (1, 2-DCE) in vitro. METHODS: Neurocytes of new born rats were cultured in vitro, which were administered with different doses of 1, 2-DCE, and NMDAR and Ca(2+) antagonists including Ketamine and Nimodiping respectively. The cell morphologic structures were observed under light microscope, and its proliferation was detected by Cell Counting Kit-VIII. RESULTS: 1, 2-DCE could damage the normal morphological structure of neurocytes: the cell body swelled and broke down, the karyon slurred or disappeared, the axone became shorten and thick, connection of neurocytes was reduced, the cell membrane was half-baked, injury of neurocytes became severer with the increase of the dose of 1, 2-DCE. There was no statistical difference in the proliferation of neurocytes between every 1, 2-DCE groups (P > 0.05), but there was significantly statistical difference between 1, 2-DCE groups, the control group, and the retarder groups (P < 0.01). CONCLUSION: 1, 2-DCE can damage the normal morphological structure of neurocytes, and the damage will become severer with the increase of the dose of 1, 2-DCE. However, the cell morphologic structures and proliferation of antagonist groups are much better than those in the 1, 2-DCE groups.