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Major depressive disorder (MDD) is a clinical condition that significantly impacts patients' physical and mental well-being, quality of life, and social functioning. The pathogenesis of MDD remains unclear, but accumulating evidence suggests a close relationship between gut microbiota and the occurrence and progression of MDD. Gut microbiota refers to the microbial community in the human intestine, which engages in bidirectional communication with the host via the "gut-brain axis" and plays a pivotal role in influencing the host's metabolism, immune system, endocrine system, and nervous system. Modulating gut microbiota entails restoring the balance and function of the intestinal flora through methods such as probiotic intake, fecal transplantation, and dietary intervention. Such modulation has been shown to effectively alleviate depressive symptoms in the host. This review synthesizes recent advancements in research on gut microbiota modulation for ameliorating depressive symptoms and can serve as a foundation for further exploration of the gut microbiota's role in MDD and its potential therapeutic benefits.
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Trastorno Depresivo Mayor , Trasplante de Microbiota Fecal , Microbioma Gastrointestinal , Probióticos , Humanos , Microbioma Gastrointestinal/fisiología , Trastorno Depresivo Mayor/microbiología , Trastorno Depresivo Mayor/terapia , Trastorno Depresivo Mayor/inmunología , Probióticos/uso terapéutico , Eje Cerebro-Intestino/fisiología , AnimalesRESUMEN
Synaptotagmin-7 (SYT7) has been proposed as an innovative therapeutic strategy for treating cognitive impairment, while its contribution to Alzheimer's disease (AD) alleviation remains unclear. In this study, we investigated the role and potential mechanisms of SYT7 in AD. APP/PS1 mice were induced as an AD mouse model, and RNA-sequencing was conducted to analyze the transcriptomic differences between the brain tissues of AD mice and controls. SYT7, which was the most significantly differentially expressed gene in the RNA-sequencing, was found to be reduced in AD-like mice, and overexpression of SYT7 alleviated cognitive dysfunction and attenuated neuroinflammation and neuronal loss in the hippocampal tissues of mice with AD. Transcription factor double-strand-break repair protein rad21 homolog (RAD21) bound to the promoter of SYT7 to activate SYT7 transcription. SYT7 and RAD21 were expressed in microglia. SYT7 and RAD21 both promoted M2 polarization of microglia, while silencing of SYT7 repressed the M2 polarization of microglia in the presence of RAD21 overexpression. Overall, our results indicate that RAD21 mediated transcriptional activation of SYT7 to promote M2 polarization of microglia, thereby alleviating AD-like symptoms in mice, which might provide prospective cues for developing therapeutic strategies to improve cognitive impairment and AD course.
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Enfermedad de Alzheimer , Microglía , Sinaptotagminas , Animales , Masculino , Ratones , Enfermedad de Alzheimer/metabolismo , Enfermedad de Alzheimer/genética , Disfunción Cognitiva/metabolismo , Modelos Animales de Enfermedad , Hipocampo/metabolismo , Ratones Transgénicos , Microglía/metabolismo , Sinaptotagminas/metabolismo , Sinaptotagminas/genéticaRESUMEN
Objectives: Disruptive mood dysregulation disorder (DMDD) is a relatively new diagnosis that comprises severe, nonepisodic irritability and recurrent outbursts of emotional instability in adolescents. This meta-analysis examined the efficacy of the available pharmacological and nonpharmacological interventions for DMDD. Methods: Literature searches were conducted in July 2023. To determine relevant articles, 330 abstracts were reviewed, and 39 articles were identified for full review. A random-effects model was used for the meta-analysis, and a subgroup analysis was performed to assess the effects of study design and intervention type. Results: Eleven studies were reviewed, including six pharmacological and five nonpharmacological. Despite high heterogeneity in effects (I2 = 85%), we showed statistically significant improvements in irritability symptoms following intervention. We showed statistically significant enhancements in symptoms of irritability following the intervention. The subgroup analysis revealed that, compared with randomized controlled trials (RCTs), open trials showed significant improvements in irritability. In addition, drug intervention significantly improved irritability compared to nondrug interventions. Atomoxetine (ATX), optimized stimulants, and stimulants combined with other drugs and behavioral therapy effectively improved irritability. Conclusions: With research indicating potential benefits for irritability from a combination of pharmacological interventions and therapy, including ATX, stimulants in conjunction with antipsychotic or antidepressant medications, and cognitive-behavioral techniques such as Dialectical Behavior Therapy for Children. Future large-scale RCTs are essential to further explore and refine these treatment approaches, especially focusing on the efficacy of combining pharmacological with effective nonpharmacological to improve irritability and overall outcomes in this population.
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Genio Irritable , Trastornos del Humor , Adolescente , Niño , Humanos , Clorhidrato de Atomoxetina/uso terapéutico , Estimulantes del Sistema Nervioso Central/uso terapéutico , Genio Irritable/efectos de los fármacos , Trastornos del Humor/tratamiento farmacológico , Trastornos del Humor/terapia , Ensayos Clínicos Controlados Aleatorios como AsuntoRESUMEN
BACKGROUND: Agomelatine (AGO) is an antidepressant with unique pharmacological effects; however, its underlying mechanisms remain unknown. In this study, we examined agomelatine's effects on catalase activity, oxidative stress, and inflammation. METHODS: Chronic restraint stress (CRS) model mice were established over 4 weeks, and AGO 50 mg/kg was administered to different groups alongside a deferasirox (DFX) 10 mg/kg gavage treatment. Behavioral tests were performed to assess the effect of AGO on the remission of depression-like behaviors. Meanwhile, the expression of CAT, the oxidative stress signaling pathway and inflammatory protein markers were assessed using ELISA, qRT-PCR, Western blot, and immunohistochemistry. RESULTS: Four weeks of AGO treatment significantly improved depression-like behavior in mice through the activation of catalase in the hippocampus and serum of the model mice, increased superoxide dismutase expression, reduced malondialdehyde expression, and reduced oxidative stress damage. Deferasirox was found to offset this therapeutic effect partially. In addition, the inflammatory pathway (including nuclear factor-κB and nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha) was not significantly altered. CONCLUSIONS: AGO can exert antidepressant effects by altering oxidative stress by modulating catalase activity.
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Antioxidantes , Depresión , Ratones , Animales , Depresión/tratamiento farmacológico , Depresión/etiología , Depresión/prevención & control , Catalasa/metabolismo , Deferasirox/farmacología , Antioxidantes/metabolismo , Estrés Oxidativo , Antidepresivos/farmacología , Antidepresivos/uso terapéuticoRESUMEN
Alzheimer's disease (AD) is one of the most common neurodegenerative diseases among the older population. Its main pathological features include the abnormal deposition of extracellular amyloid-ß plaques and the intracellular neurofibrillary tangles of tau proteins. Its clinical presentation is complex. This review introduces the pathological processes in AD and other common neurodegenerative diseases. It then discusses the positron emission tomography (PET) probes that target amyloid-ß plaques and tau proteins for diagnosing AD. According to the A/T(N) research framework, combined targeted amyloid-ß and tau protein detection via PET to further improve the diagnostic accuracy of AD. In particular, the properties of the 18F-flortaucipir and 18F-MK6240 tracers-may be more beneficial in helping to differentiate AD from other common neurodegenerative diseases, such as dementia with Lewy bodies, Parkinson's disease dementia, and frontotemporal dementia. Furthermore, the A/T(N) research framework should be used as the clinical diagnosis model of AD in the future.
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Enfermedad de Alzheimer , Demencia Frontotemporal , Enfermedades Neurodegenerativas , Enfermedad de Parkinson , Humanos , Enfermedad de Alzheimer/diagnóstico por imagen , Proteínas tau , Péptidos beta-Amiloides/metabolismo , Diagnóstico Diferencial , Enfermedad de Parkinson/patología , Tomografía de Emisión de Positrones/métodosRESUMEN
Mild behavioral impairment (MBI) is a neurobehavioral syndrome that occurs in the absence of cognitive impairment later in life (≥50 years of age). MBI is widespread in the pre-dementia stage and is closely associated with the progression of cognitive impairment, reflecting the neurobehavioral axis of pre-dementia risk states and complementing the traditional neurocognitive axis. Despite being the most common type of dementia, Alzheimer's disease (AD) does not yet have an effective treatment; therefore, early recognition and intervention are crucial. The Mild Behavioral Impairment Checklist is an effective tool for identifying MBI cases and helps identify people at risk of developing dementia. However, because the concept of MBI is still quite new, the overall understanding of it is relatively insufficient, especially in AD. Therefore, this review examines the current evidence from cognitive function, neuroimaging, and neuropathology that suggests the potential use of MBI as a risk indicator in preclinical AD.
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Alzheimer's disease (AD) or vestibular dysfunction may impair visual-spatial cognitive function. Recent studies have shown that vestibular dysfunction is increasingly common in patients with AD, and patients with AD with vestibular impairment show more visual-spatial cognitive impairment. By exploring the relationship and interaction mechanism among the vestibular system, visual-spatial cognitive ability, and AD, this study aims to provide new insights for the screening, diagnosis, and rehabilitation intervention of patients with AD. In contrast, routine vestibular function tests are particularly important for understanding the vestibular function of patients with AD. The efficacy of vestibular function test as a tool for the early screening of patients with AD must also be further studied. Through the visual-spatial cognitive ability test, the "spatial impairment" subtype of patients with AD, which may be significant in caring for patients with AD to prevent loss and falls, can also be determined. Additionally, the visual-spatial cognitive ability test has great benefits in preventing and alleviating cognitive decline of patients with AD.
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Objective: Static regional homogeneity (ReHo) based on the resting-state functional magnetic resonance imaging (rs-fMRI) has been used to study intrinsic brain activity (IBA) in Alzheimer's disease (AD). However, few studies have examined dynamic ReHo (dReHo) in AD. In this study, we used rs-fMRI and dReHo to investigate the alterations in dynamic IBA in patients with AD to uncover dynamic imaging markers of AD. Method: In total, 111 patients with AD, 29 patients with mild cognitive impairment (MCI), and 73 healthy controls (HCs) were recruited for this study ultimately. After the rs-fMRI scan, we calculated the dReHo values using the sliding window method. ANOVA and post hoc two-sample t-tests were used to detect the differences among the three groups. We used the mini-mental state examination (MMSE) and Montreal Cognitive Assessment (MoCA) to evaluate the cognitive function of the subjects. The associations between the MMSE score, MoCA score, and dReHo were assessed by the Pearson correlation analysis. Results: Significant dReHo variability in the right middle frontal gyrus (MFG) and right posterior cingulate gyrus (PCG) was detected in the three groups through ANOVA. In post hoc analysis, the AD group exhibited significantly greater dReHo variability in the right MFG than the MCI group. Compared with the HC group, the AD group exhibited significantly increased dReHo variability in the right PCG. Furthermore, dReHo variability in the right PCG was significantly negatively correlated with the MMSE and MoCA scores of patients with AD. Conclusion: Disrupted dynamic IBA in the DMN might be an important characteristic of AD and could be a potential biomarker for the diagnosis or prognosis of AD.
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INTRODUCTION: Depression is a class of important mental illness, which has become a severe health problem perplexing the world due to its high morbidity rate, high disability rate, and great disease burden. This study aimed to evaluate the role and possible mechanisms of P2RY12 in the depression-like behaviors model. METHODS: Serum samples of patients with depression-like behaviors were used to analyze the expression of P2RY12. Models of mice were given LPS via intraperitoneal injection for 7 days. Behavioral tests were executed in this experiment. RESULTS: The expression of P2RY12 in models of depression-like behaviors or mice with depression- like behaviors were induced. The inhibition of P2RY12 presents depression-like behaviors and reduces inflammation in the model of depression-like behaviors. P2RY12 induced NLRP3 expression and suppressed NLRP3 ubiquitination in a model of depression-like behavior. The inhibition of NLRP3 reduced the effects of P2RY12 in mice model of depression-like behaviors. The regulation of NLRP3 controlled the effects of the P2RY12 in vitro model of depression-like behaviors. CONCLUSION: We conclude that P2RY12 increased neuroinflammation to accelerate depression-like behaviors by NLPR3 inflammasome, providing novel information for the treatment of depressionlike behaviors.
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Depresión , Inflamasomas , Ratones , Animales , Inflamasomas/metabolismo , Depresión/tratamiento farmacológico , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Enfermedades Neuroinflamatorias , Inflamación , Lipopolisacáridos/toxicidad , Receptores Purinérgicos P2Y12RESUMEN
BACKGROUND: Treatment-resistant schizophrenia is a severe form of schizophrenia characterized by poor response to at least two antipsychotic drugs and is typically treated with clozapine. However, clozapine lowers the epileptic threshold, leading to seizures, which are severe side effects of antipsychotics that result in multiple complications. Clozapine-related seizures are generally considered to be dose-dependent and especially rare in the low-dose (150-300 mg/d) clozapine treated population. Due to clinical rarity, little is known about its clinical characteristics and treatment. CASE SUMMARY: A 62-year-old Chinese man with a 40-year history of treatment-resistant schizophrenia presented to the Emergency Department with symptoms of myoclonus, consciousness disturbance and vomiting after taking 125 mg clozapine. Upon admission, the patient had a suddenly generalized tonic-clonic seizure lasting for about half a minute with persistent disturbance of consciousness, fever, cough and bloody sputum, which was considered to be low-dose clozapine-related seizure. After antiepileptic and multiple anti-infection treatments, the patient was discharged without epileptic or psychotic symptoms. CONCLUSION: Our aim is to highlight the early prevention and optimal treatment of clozapine-related seizure through case analysis and literature review.
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Alzheimer's disease (AD) is the most common cognitive disorder in the elderly. Its main clinical manifestations are cognitive decline (C), behavioral and psychological symptoms (B), and a decline in the activities of daily living (A), also known as ABC symptoms. Early identification and evaluation of ABC symptoms are helpful for establishing the accurate diagnosis, comprehensive treatment, and prognosis of AD. To guide Chinese clinical practice for optimization of the comprehensive management of AD, in 2018, The Academy of Cognitive Disorder of China gathered 22 neurologists and gerontologists in China to build a consensus on the comprehensive management of AD. Based on a review of the evidence, the consensus summarizes the pathogenesis, pathological changes, clinical manifestations, evaluation, diagnosis, drug and non-drug treatment, and patient care for AD. Focus group discussion was used to establish a flowchart of comprehensive ABC management for AD patients. The new consensus provides a feasible AD management process for clinicians.
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Actividades Cotidianas , Enfermedad de Alzheimer , Anciano , Enfermedad de Alzheimer/complicaciones , Enfermedad de Alzheimer/terapia , China , Cognición , Consenso , HumanosRESUMEN
Stroke is a global health problem, and survivors of a stroke often suffer from cognitive impairment, which has an essential impact on the rehabilitation of various functions. Repetitive Transcranial Magnetic Stimulation (rTMS) has been widely used in the rehabilitation treatment of stroke patients. There are many investigations into how rTMS impacts motor dysfunction, speech dysfunction and swallowing dysfunction after stroke, but the analysis of rehabilitation effect on stroke patients with cognitive dysfunction is lacking. The purpose of this study was to analyze the effect of different rTMS related therapies on cognitive impairment and to evaluate its clinical effect on cognitive rehabilitation after stroke. Four databases including PubMed, EMBASE, MEDLINE and the Cochrane Library, were searched and a total of 2754 papers were collected. Two reviewers independently completed a review of all papers' titles and abstracts, screened out the documents that met the criteria, and carried out data extraction, quality assessment, and data analysis. A total of six studies with 197 patients were included. Three studies used the Mini-Mental Status Examination (MMSE) scale to evaluate the cognitive function with a mean effect size of 1.89 (95% CI = -3.08-6.86). Two studies used the Loewenstein Occupational Therapy of Cognitive Assessment (LOTCA) scale with the mean effect size of 1.64 (95% CI = -7.65-10.93). These studies were evaluated separately. Our article provides that rTMS has a positive effect on improving the cognitive ability of stroke patients, but the evidence is still limited, and further large-scale studies are needed to explore the optimal stimulus parameters.
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Disfunción Cognitiva , Rehabilitación de Accidente Cerebrovascular , Accidente Cerebrovascular , Cognición , Disfunción Cognitiva/etiología , Disfunción Cognitiva/terapia , Humanos , Accidente Cerebrovascular/complicaciones , Accidente Cerebrovascular/terapia , Estimulación Magnética TranscranealRESUMEN
Retraction of: 'Inhibitory effect of Aphidicolin - a tetracyclic diterpene - on the proliferation and apoptotic induction in human cervical cancer (HeLa) cells', by En-Yan Yu, Rui-Yan Zhao, Dong-Sheng Wang, JBUON 2015;20(6):1480-1486; PMID:26854444. Following the publication of the above article, readers drew to our attention that part of the data was unreliable. The authors were requested to provide the raw data to prove the originality, but were unable to do so. After an investigation, the Editors of JBUON decided to retract this article. We thank the readers for bringing this matter to our attention. We apologize for any inconvenience it may cause.
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BACKGROUND: As a potential brain imaging biomarker, amplitude of low frequency fluctuation (ALFF) has been used as a feature to distinguish patients with Alzheimer's disease (AD) and amnestic mild cognitive impairment (aMCI) from normal controls (NC). However, it remains unclear whether the frequency-dependent pattern of ALFF alterations can effectively distinguish the different phases of the disease. METHODS: In the present study, 52 AD and 50 aMCI patients were enrolled together with 43 NC in total. The ALFF values were calculated in the following three frequency bands: classical (0.01-0.08 Hz), slow-4 (0.027-0.073 Hz) and slow-5 (0.01-0.027 Hz) for the three different groups. Subsequently, the local functional abnormalities were employed as features to examine the effect of classification among AD, aMCI and NC using a support vector machine (SVM). RESULTS: We found that the among-group differences of ALFF in the different frequency bands were mainly located in the left hippocampus (HP), right HP, bilateral posterior cingulate cortex (PCC) and bilateral precuneus (PCu), left angular gyrus (AG) and left medial prefrontal cortex (mPFC). When the local functional abnormalities were employed as features, we identified that the ALFF in the slow-5 frequency band showed the highest accuracy to distinguish among the three groups. CONCLUSION: These findings may deepen our understanding of the pathogenesis of AD and suggest that slow-5 frequency band may be helpful to explore the pathogenesis and distinguish the phases of this disease.
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BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by memory impairment. Previous studies have largely focused on alterations of static brain activity occurring in patients with AD. Few studies to date have explored the characteristics of dynamic brain activity in cognitive impairment, and their predictive ability in AD patients. METHODS: One hundred and eleven AD patients, 29 MCI patients, and 73 healthy controls (HC) were recruited. The dynamic amplitude of low-frequency fluctuation (dALFF) and the dynamic fraction amplitude of low-frequency fluctuation (dfALFF) were used to assess the temporal variability of local brain activity in patients with AD or mild cognitive impairment (MCI). Pearson's correlation coefficients were calculated between the metrics and subjects' behavioral scores. RESULTS: The results of analysis of variance indicated that the AD, MCI, and HC groups showed significant variability of dALFF in the cerebellar posterior and middle temporal lobes. In AD patients, these brain regions had high dALFF variability. Significant dfALFF variability was found between the three groups in the left calcarine cortex and white matter. The AD group showed lower dfALFF than the MCI group in the left calcarine cortex. CONCLUSIONS: Compared to HC, AD patients were found to have increased dALFF variability in the cerebellar posterior and temporal lobes. This abnormal pattern may diminish the capacity of the cerebellum and temporal lobes to participate in the cerebrocerebellar circuits and default mode network (DMN), which regulate cognition and emotion in AD. The findings above indicate that the analysis of dALFF and dfALFF based on functional magnetic resonance imaging data may give a new insight into the neurophysiological mechanisms of AD.
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BACKGROUND: To study the efficacy of tandospirone citrate in treating Alzheimer's disease (AD) patients with anxiety. METHODS: Thirty mild-to-moderate AD patients with anxiety symptoms were randomly divided into a monotherapy group (donepezil) and a combination therapy group (donepezil and tandospirone). The treatment lasted for 12 weeks. Drug efficacy was regularly assessed using psychological assessment scales and quantitative pharmaco-electroencephalogram (QPEEG) power spectral analysis. RESULTS: After 12 weeks of treatment, the mean Hamilton Anxiety Scale (HAMA) score and mean Neuropsychiatric Inventory (NPI) score of the combination therapy group were 5.13±4.18 and 4.2±5.0, respectively, which was significantly lower compared to baseline and the monotherapy group (all P<0.05). The mean attention score on the Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-Cog) was 0.07±0.26 for the combination group, which was significantly lower than that of the monotherapy group (P<0.05). QPEEG revealed that the power values of the δ wave in the right prefrontal lobe, left middle temporal lobe and right posterior temporal lobe decreased in the combination therapy group but not in the monotherapy group. Similarly, the power values of the α2 wave in the right parietal, right posterior temporal and left middle temporal lobes, and the ß1 wave power values of left middle temporal and left posterior temporal lobes were also significantly decreased in the combination therapy group, but not in the monotherapy group. CONCLUSIONS: Tandospirone citrate can significantly improve anxiety symptoms and attention in patients with mild to moderate AD. QPEEG examination might provide a objective way for the efficacy of the tandospirone in anxiety symptoms of the patients with Alzheimer's disease.
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BACKGROUND: Alzheimer's disease (AD) is an age-progressive neurodegenerative disorder that affects cognitive function. There have been several functional connectivity (FC) strengths; however, FC density needs more development in AD. Therefore, this study wanted to determine the alternations in resting-state functional connectivity density (FCD) induced by Alzheimer's and mild cognitive impairment (MCI). METHODS: One hundred and eleven AD patients, 29 MCI patients, and 73 healthy controls (age- and sex-matched) were recruited and assessed using resting-state functional magnetic resonance imaging (MRI) scanning. The ultra-fast graph theory called FCD mapping was used to calculate the voxel-wise short- and long-range FCD values of the brain. We performed voxel-based between-group comparisons of FCD values to show the cerebral regions with significant FCD alterations. We performed Pearson's correlation analyses between aberrant functional connectivity densities and several clinical variables with adjustment for age and sex. RESULTS: Patients with cognition decline showed significantly abnormal long-range FCD in the cerebellum crus I, right insula, left inferior frontal gyrus, left superior frontal gyrus, left inferior frontal gyrus, and right middle frontal gyrus. The short-range FCD changed in the cerebellum crus I, left inferior frontal gyrus, left superior occipital gyrus, and right middle frontal gyrus. The long- and short-range functional connectivity in the left inferior frontal gyrus was positively correlated with Mini-mental State Examination (MMSE) scores. CONCLUSIONS: FCD in the identified regions reflects mechanism and compensation for loss of cognitive function. These findings could improve the pathology of AD and MCI and supply a neuroimaging marker for AD and MCI.
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Cancer-related cognitive impairment (CRCI) refers to a series of cognitive impairment symptoms associated with alternations in brain structure and function, caused by a non-central nervous system malignant tumor and its related treatment. CRCI may present as memory loss, impaired concentration, difficulty in multitasking and word retrieval, and reduced comprehension speed. CRCI has become one of the prevalent factors that compromise the quality of life for cancer survivors. Different treatments, including surgery, chemotherapy, radiotherapy, endocrine therapy, and targeted drugs, may contribute to CRCI. Meanwhile, patients' factors, including emotional challenges and genetic makeup, also contribute to the development of CRCI. The condition can be treated with using stimulants methylphenidate and modafinil, metabolites of nicotine: cotinine, antidepressants of fluoxetine and fluvoxamine, dementia drug of donepezil, and antioxidants ZnSO4, n-acetyl cysteine, propofol, and Chinese herbal of silver leaf medicine. Psychotherapies, including meditation and relaxation, cognitive rehabilitation training, along with physical therapies, including aerobic exercise, resistance training, balance training, yoga, qigong, tai chi electroencephalogram biofeedback, and acupuncture, are also beneficial in alleviating cancer-related cognitive impairment symptoms. In recent years, researchers have focused on factors related to the condition and on the available interventions. However, most research was conducted independently, and no review has yet summarized the latest findings. This review details and discusses the status of related factors and potential treatments for CRCI. We also supply specific recommendations to facilitate future research and integration in this field.
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To discuss the changes in cognitive function and related brain regions in patients with chronic benzene poisoning. Few studies have explored the damage to cognitive function that occurs in benzene toxic encephalopathy. It is important to identify early in the course of disease whether cognitive dysfunction is caused by benzene poisoning so that disease prognosis and appropriate treatment can be determined. We reported on the chronic benzene poisoning of a 41-year-old Han Chinese woman. The patient had graduated from primary school, and she had a cheerful and diligent personality. She had performed painting work for more than five years, and her primary work involved painting swivel chairs. The primary reasons she attended the psychiatric clinic were loss of appetite, she had experienced fatigue for more than 2 months, and she had had memory loss for a month. These symptoms seriously impacted the patient's daily life and ability to work. The patient's husband expressed concern that she could not recognize acquaintances, could not find her way home, and had lost approximately 5 kg per month over two months. We analyzed changes in this chronic benzene poisoning patient's cognitive function with cognitive function assessments and magnetic resonance imaging (MRI). Measurements were taken on presentation to hospital, during the patient's hospitalization, and three months following discharge. Long-term exposure to benzene can damage the central nervous system. However, it is difficult to recognize when cognitive impairment is caused by chronic benzene poisoning, as it rarely presents with a decline in cognitive function as the primary clinical manifestation. Atypical symptoms, such as decreased immune function and gastrointestinal issues, may be the first symptoms to appear, and these atypical symptoms are difficult to detect in the early stages of disease. Regular screening of high-risk groups is required to significantly reduce the incidence of systemic damage caused by benzene poisoning.