Reversible Cognitive Impairment Research Articles

Role of Probiotic Strain Lactobacillus acidophilus in the Reversal of Gut Dysbiosis Induced Brain Cognitive Decline

In the central nervous system, bidirectional communication between the brain and gut results in memory formation due to synaptic plasticity changes. During a healthy state, oral balanced microflora plays a pivotal role in memory formation by inhibiting the enterotoxin level produced by infectious pathogens. In disease conditions, beneficial microbial dysbiosis may result in excess enterotoxin production. Further, excess enterotoxin secretion prevents beneficial bacteria's proliferation and impairs neurotransmitter precursor compounds' transport to the brain. Blockade of neurotransmitter precursor compounds may result in the development of memory loss. The present study stated the role of Lactobacillus acidophilus in recovering memory loss. Reversal of cognitive impairment is shown with the help of a three-step behavioural analysis, which consists of one pre-infusive behavioural analysis and two post-infusive behavioural analyses (phase 1 and 2). The pre-infusive analysis showed no cognitive impairment in an assimilated environment without any infusions. After oral microbial infusions, phase 1 of post-infusive behavioural analysis showed the presence of cognitive impairment in the experimental groups who received oral infusions. Formed cognitive impairment is reverted with the help of L. acidophilus oral infusion in phase 2 of post-infusive analysis. Comparative three-step behavioural analysis proved that Pseudomonas aeuroginosa induced cognitive impairment may revert to normal conditions with the help of L. acidophilus. The outcome of the present study proves that cognitive impairment developed due to poor oral hygiene can be treated with the help of probiotic microorganisms.

Validity and performance of cognitive scales in elderly patients with depression in a tertiary care hospital in Chennai

Background: Late-life depression in older adults can cause reversible cognitive impairment, often resulting in pseudo-dementia. Cognitive impairment can lead to executive dysfunction, reduced flexibility, and difficulty thinking and decision-making. This study aimed to assess the validity and performance of cognitive scales in late-life depression among patients attending the outpatient department of the institute of mental health, Chennai. Methods: This prospective study included 360 patients aged >50 years who were diagnosed with depression and attended the OPD at the institute of mental health, Chennai. Baseline assessments were performed at the time of recruitment into the study (visit 1), and scheduled visits were performed every six months for two years (visits 2 to 5). Unscheduled visits were done every month, and adverse events were monitored and recorded periodically Results: Among 59 patients, 53.1% were female, 32.2% were diabetic, and 93.9% were experiencing subjective working difficulties. The Montreal cognitive assessment scale classified 51.4% as moderate, while the ADAS-cog and ACE scales classified 86% and 99.7%, respectively, as having abnormal mental status. However, a significant correlation and discrepancy between scores were observed for scales such as ACE, ADAS-cog, standardised mini-mental status examination, and Montreal cognitive assessment scale. A strong correlation was found between ACE, MMSE, MoCA, and ACE; however, FAST showed a significant negative correlation. The MoCA was strongly correlated with the MMSE, ACE, ADAS-cog, and Mini-Cog, indicating good alignment with the FAST. Conclusions: Cognitive scales strongly correlate with late-life depression in patients, suggesting an improvement in assessment, evaluation, and treatment to address cognitive deficits.

Prevalence and related factors of cognitive frailty in diabetic patients in China: a systematic review and meta-analysis.

Cognitive frailty (CF) is characterized by physical frailty and potentially reversible cognitive impairment without Alzheimer's disease and other dementias. Clarifying the prevalence and related factors of cognitive frailty can help researchers understand its epidemiological status and formulate intervention measures. This study aims to conduct a systematic review and meta-analysis of the prevalence and related factors of CF in diabetic patients in Chinas to better understand the current status of CF in diabetic patients in China and develop effective intervention measures for related factors. PubMed, Web of Science, Embase, Cochrane Library, CNKI, Weipu(VIP), WANFANG, China Biology Medicine (CBM) and DUXIU were searched to collect epidemiological data on Chinese diabetic patients. Articles published through May 29, 2023, were searched. The number of diabetes with CF and the total number of diabetes in the included studies were extracted to estimate the prevalence of diabetes with CF. For factors related to diabetes with CF, odds ratios (OR) and 95% confidence intervals (CI) were used for estimation. A total of 248 records were screened, of which 18 met the inclusion criteria. The results of meta-analysis showed that the prevalence of Chinese diabetic patients with CF was 25.8% (95% CI = 19.7 to 31.9%). Subgroup analysis showed that hospital prevalence was higher than in the community and in women than in men. Combined estimates showed that depression, malnutrition, advanced age (≥70, ≥80), combined chronic diseases ≥4 and glycated hemoglobin ≥8.5 were risk factors for CF in diabetics patients in China, with regular exercise and high education level (≥ college) as protective factors. Cognitive frailty was common in diabetic patients in China. Such populations should be screened early and intervened with relevant factors.Systematic review registration: A systematic review of this study evaluated the registered websites as https://www.crd.york.ac.uk/PROSPERO/, CRD42023431396.

Transcranial Electromagnetic Wave Treatment: A Fountain of Healthy Longevity?

Most diseases of older age have as their common denominator a dysfunctional immune system, wherein a low, chronic level of inflammation is present due to an imbalance of pro-inflammatory cytokines over anti-inflammatory cytokines that develops during aging (“inflamm-aging”). A gerotherapeutic that can restore the immune balance to that shared by young/middle-aged adults and many centenarians could reduce the risk of those age-related diseases and increase healthy longevity. In this perspectives paper, we discuss potential longevity interventions that are being evaluated and compare them to a novel gerotherapeutic currently being evaluated in humans—Transcranial Electromagnetic Wave Treatment (TEMT). TEMT is provided non-invasively and safety through a novel bioengineered medical device—the MemorEM—that allows for near complete mobility during in-home treatments. Daily TEMT to mild/moderate Alzheimer’s Disease (AD) patients over a 2-month period rebalanced 11 of 12 cytokines in blood back to that of normal aged adults. A very similar TEMT-induced rebalancing of cytokines occurred in the CSF/brain for essentially all seven measurable cytokines. Overall inflammation in both blood and brain was dramatically reduced by TEMT over a 14–27 month period, as measured by C-Reactive Protein. In these same AD patients, a reversal of cognitive impairment was observed at 2 months into treatment, while cognitive decline was stopped over a 2½ year period of TEMT. Since most age-related diseases have the commonality of immune imbalance, it is reasonable to postulate that TEMT could rebalance the immune system in many age-related diseases as it appears to do in AD. We propose that TEMT has the potential to reduce the risk/severity of age-related diseases by rejuvenating the immune system to a younger age, resulting in reduced brain/body inflammation and a substantial increase in healthy longevity.

Scopolamine causes delirium-like brain network dysfunction and reversible cognitive impairment without neuronal loss.

Delirium is a severe acute neuropsychiatric syndrome that commonly occurs in the elderly and is considered an independent risk factor for later dementia. However, given its inherent complexity, few animal models of delirium have been established and the mechanism underlying the onset of delirium remains elusive. Here, we conducted a comparison of three mouse models of delirium induced by clinically relevant risk factors, including anesthesia with surgery (AS), systemic inflammation, and neurotransmission modulation. We found that both bacterial lipopolysaccharide (LPS) and cholinergic receptor antagonist scopolamine (Scop) induction reduced neuronal activities in the delirium-related brain network, with the latter presenting a similar pattern of reduction as found in delirium patients. Consistently, Scop injection resulted in reversible cognitive impairment with hyperactive behavior. No loss of cholinergic neurons was found with treatment, but hippocampal synaptic functions were affected. These findings provide further clues regarding the mechanism underlying delirium onset and demonstrate the successful application of the Scop injection model in mimicking delirium-like phenotypes in mice.

Prevalence of Depressive Symptoms in a Memory Clinic Cohort: A Retrospective Study

Background: Depression has been suggested to be a cause of reversible cognitive impairment but also a risk factor for neurodegenerative disease. Studies suggest that depression prevalence may be high in early onset dementia, particularly Alzheimer’s disease, but this has not been systematically assessed in a biomarker-validated clinical dementia cohort to date. Objective: To examine the prevalence, features, and association with amyloid pathology of lifetime depressive symptoms in a memory clinic cohort meeting appropriate use criteria for amyloid PET imaging. Methods: We included 300 patients from a single-center memory clinic cohort that received diagnostic biomarker evaluation with amyloid PET imaging according to appropriate use criteria. History of lifetime depressive symptoms was retrospectively assessed through structured review of clinical correspondence. Results: One hundred forty-two (47%) patients had a history of significant depressive symptoms (‘D+’). Of these, 89% had ongoing symptoms and 60% were on antidepressants at the time of presentation to our Clinic. Depressive symptoms were equally highly prevalent in the amyloid-positive and the heterogeneous group of amyloid-negative patients. Conclusion: Approximately half of patients who meet appropriate use criteria for amyloid PET have a history of depressive symptoms. We suggest that depression is an important feature of both neurodegenerative and non-neurodegenerative cognitive impairment and may contribute to the diagnostic uncertainty behind referral to amyloid PET.

Neuroprotective effect of mildronate and L-carnitine on the cognitive parameters of aged mice and mice with LPS-induced inflammation.

Mildronate (MD) is a cardioprotective drug used for the treatment of cardiovascular diseases by switching metabolism from the fatty acids to glucose oxidation. This effect is achieved via inhibition of synthesis of L-carnitine (L-car), a common supplement, which is used for improving of fatty acid metabolism. Both MD and L-car have similar neuroprotective effect. Our goal was to investigate the effect of two drugs on the cognitive parameters of mice under different conditions (aging and lipopolysaccharide (LPS)-induced inflammation). We showed that L-car partly improved the memory and decreased the extent of mtDNA damage in the hippocampus of mice with the LPS-induced inflammation. L-car induced mitochondrial biogenesis and mitophagy in the Nrf2-dependent manner. Both MD and L-car upregulated expression of genes involved in the mitochondrial quality control. In 15-month-old mice, MD improved long-term and short-term memory, reduced the extent of mtDNA damage, and decreased the concentration of diene conjugates in the hippocampus in the Nrf2-independent manner. L-car as a Nrf2 activator had a better neuroprotective effect by normalizing mitochondrial quality control in the reversible cognitive impairment caused by the LPS-induced inflammation, while MD had a better neuroprotective effect in the irreversible cognitive impairment in aged mice, possibly due to a deeper restructuring of metabolism and reduction of oxidative stress.

Subclinical Hypothyroidism and Cognitive Impairment.

Although thyroid dysfunction has been considered as a cause of reversible cognitive impairment, association between subclinical hypothyroidism and cognitive impairment is controversial. We compared cognitive profiles of patients in an euthyroid or subclinical hypothyroid (sHypo) state, as well as their disease progression from mild cognitive impairment (MCI) to dementia within 3 years. We included 2,181 patients in a euthyroid and 284 in a sHypo state over 60 years of age who underwent an extensive cognitive assessment at Seoul National University Bundang Hospital but were not prescribed levothyroxine, methimazole, carbimazole, or propylthiouracil. After propensity score matching for age, sex, and education level, 1,118 patients in a euthyroid and 283 patients in a sHypo state were included. Attention, language, memory, visuocontructive, and executive functions were compared between the groups using Student's t-test or the Mann-Whitney U test. To investigate the association between disease progression and subclinical hypothyroidism, a Cox regression analyses was performed in 379 patients with MCI. Patients with thyroid-stimulating hormone levels over 10 mlU/L was classified as the "sHypo10", and hazard ratios for sHypo or sHypo10 were assessed. There was no difference in attention, language, memory, visuoconstructive, and executive functions between the patient groups. Progression from MCI to dementia was not associated with sHypo or sHypo10. There was no difference in cognitive profile between euthyroid and sHypo patients, and no association between subclinical hypothyroidism and disease progression. This might suggest a clue of strategies regarding hormone therapy in subclinical hypothyroidism with cognitive impairment.

Reversible cognitive impairment and parkinsonism with leukoencephalopathy due to cranial dural arteriovenous fistula

Parkinsonism and rapid cognitive impairment may have many causes, but only a few have specific treatment. Cranial dural arteriovenous fistula (DAVF) represents 10-15% of intracranial arteriovenous malformations. Clinical manifestations depend on location and venous drainage. It is common the presence of pulsatile tinnitus, bruits and headache or headache and papilledema. Progressive cognitive decline is an unusual presentation due to bilateral thalamic edema or cortical venous hypertension. Endovascular or surgical treatment can reverse disease symptoms.We present a 74-year old man with rapidly progressive cognitive impairment and parkinsonism and a subsequent diagnosis of dural arteriovenous fistula (DAVF). Brain MRI revealed diffuse leukoencephalopathy probably attributable to elevated venous pressure. He was treated with partial embolization with Onix and left transverse sinus angioplasty. Following the procedure, there was a substantial reduction of venous pressure signs and remarkable clinical and imaging improvement, persisting at two years follow-up. This case represents an unusual presentation of DAVF. It is important to suspect the diagnosis of DAVF in cases with rapidly evolving cognitive impairment, parkinsonism and leukoencephalopathy as it can be reversible with early treatment.

Reversible Dysexecutive Syndrome From CSF Overshunting in a Patient With Normal Pressure Hydrocephalus.

A 72-year-old male science teacher with normal pressure hydrocephalus presented 1 year after ventriculoperitoneal (VP) shunt placement with neck pain, behavioral changes, and nonamnestic cognitive decline. Six months prior, his shunt was adjusted from 4 to 3. Montreal Cognitive Assessment was 21/30 with dysexecutive predominance. EEG was unremarkable. CSF Alzheimer disease biomarkers were borderline. MRI (Figure 1) found overshunting. After shunt adjustments (3–4), his cognitive and behavioral symptoms resolved. Repeat Montreal Cognitive Assessment after 4 months was 29/30 with sustained remission after 1 year. Intracranial hypotension, whether from VP shunting or spontaneous CSF leak,1,2 may cause reversible dysexecutive cognitive impairment.

Vascular intracranial malformations and dementia: An under-estimated cause and clinical correlation. Clinical note

Cerebrovascular malformations (CVMs) such as arteriovenous malformations (AVMs) or dural arteriovenous fistulas (DAVFs) represent a possible source of intracranial hemorrhage, but these malformations can also manifest with neurologic disorders secondary to ischemic penumbra from vascular steal. In the latter case, the clinical manifestations are less obvious and characteristic, and may include a varied clinical spectrum ranging from focal deficits to generalized malfunction of the brain parenchyma resulting in dementia. Dementias secondary to CVMs constitute a probably underestimated subpopulation of patients of great interest because they present with devastating but potentially reversible cognitive impairment. We examined the pertinent literature regarding the clinical manifestations of CVMs characterized by cognitive impairment and describe the distinctive clinical features. Our results confirm that cognitive impairment is one of the clinical manifestations of CVMs and is a frequently misrecognized and often late-diagnosed cause of reversible dementia.

S2893 A Clinical Quandary: Reversible Trientine-Associated Cognitive Impairment in the Treatment of Wilson’s Disease

S2893 A Clinical Quandary: Reversible Trientine-Associated Cognitive Impairment in the Treatment of Wilson’s Disease

The sTREM2 Concentrations in the Blood: A Marker of Neurodegeneration?

Microglia performs a variety of functions during brain development designed to maintain brain homeostasis. Triggering receptor expressed on myeloid cells 2 (TREM2) is expressed in microglial cells modulating phagocytosis, cytokine production, cell proliferation, and cell survival. Interestingly, the levels of soluble TREM2 (the secreted ectodomain of TREM2, sTREM2) were higher in cerebrospinal fluid (CSF) from Alzheimer's disease (AD) patients than subjects without cognitive decline. It is noteworthy that, while CSF sTREM2 levels have been extensively studied, few studies have investigated sTREM2 in blood producing conflicting results. We aimed to investigate the levels of sTREM2 in CSF and blood from a cohort of well-characterized AD comparing the results to those obtained in patients suffering from idiopathic normal pressure hydrocephalus (iNPH), a potentially reversible cognitive impairment. Our findings underlined a significantly lower plasma sTREM2 concentration in AD patients compared to iNPH subjects [39.1 ng/mL (standard deviation (SD), 15.0) and 47.2 ng/mL (SD, 19.5), respectively; p = 0.01], whereas no difference was revealed between the two groups in the CSF sTREM2 levels. The adjusted regression analyses evidenced in AD patients an association between plasma and CSF sTREM2 levels [B = 0.411; 95% confidence interval (CI), 0.137–0.685, p = 0.004], as well as β-amyloid concentrations (B = 0.035; 95% CI, 0.007–0.063, p = 0.01) and an association between CSF sTREM2 and phospho-Tau concentrations (B = 0.248; 95% CI, 0.053–0.443; p = 0.01). No significant relation was found in iNPH patients. In conclusion, these differences in sTREM2 profiles between AD and iNPH reinforce the notion that this receptor has a role in neurodegeneration.

Disfunção Cognitiva na Depressão: O Triste Esquecimento

INTRODUÇÃO: Aproximadamente 30% a 40% dos idosos com depressão apresentam sintomas cognitivos reversíveis, vulgarmente denominada de pseudodemência, que corresponde à condição tratável mais vezes confundida com demência.O nosso objetivo foi rever a evidência existente sobre a disfunção cognitiva na depressão e as principais diferenças no diagnóstico, abordagem e prognóstico, comparativamente à demência.METODOLOGIA: Revisão da literatura usando os seguintes termos MeSH: “Depressive Disorder”, “Cognitive Dysfunction” e “Dementia”.RESULTADOS E CONCLUSÃO: Diversas situações podem cursar com défices cognitivos, sendo essencial colher uma história clínica completa e avaliar o estado funcional basal do doente. O exame neurológico deve ser sempre realizado, assim como excluídas as principais causas orgânicas de défice cognitivo. O papel do médico de família é importante na orientação do doente com queixas mnésicas e sintomatologia depressiva, podendo implicar, em alguns casos, uma abordagem multidisciplinar entre a Medicina Geral e Familiar, a Psiquiatria e a Neurologia.

Evaluation of neuroprotective potential of methanolic extract of Hemidesmus indicus extract in Aβ (1-42) induced rats

Excessive cerebral deposition of amyloid-beta (Aβ) peptides with 40-42 amino acids are the major neuropathologic feature of Alzheimer's Disease (AD), accompanied by a progressive and functional decline in cognition. With the failing attempts in the development of new pharmacological intervention and due to suboptimal results from the existing therapies available for the treatment of AD, there is a constant hunt for a new therapeutic alternative to address this severe neurodegenerative disease. The present study aimed to investigate the neuroprotective effect of Hemidesmus indicus extract in Aβ (1-42) infused model of AD. Sporadic model of AD was achieved by intracerebroventricular (i.c.v) injection of Aβ (1-42) peptide in Wistar rats, followed by treatment with methanolic extract of H. indicus (MEHI) at 100 and 200 mg/kg for 28 days. Locomotor activity, Radial arm Maze task and Passive avoidance test were used for the assessment of neurobehavioral deficits. After completion of 28 days treatment protocol, animals were euthanized and brains were collected for neurochemical analysis. Reversal of cognitive impairment was observed by MEHI on Aβ (1-42) rats, as evidenced by improved spatial memory learning. Furthermore, MEHI attenuated Aβ (1-42) induced oxidative stress and inhibited acetylcholine esterase (AChE) activity. Collectively, these findings exhibited neuroprotective activity of MEHI by ameliorating Aβ (1-42) mediated neuronal damage, thereby can stand as a potential disease-modifying therapeutic for curbing AD pathology.

Prediction of cognitive response to surgery in elderly patients with primary hyperparathyroidism

BackgroundPrimary hyperparathyroidism (pHPT) can be associated with potentially reversible cognitive impairment, which is occasionally mistaken for natural ageing and dementia. The aim was to evaluate short-term medical normalization of hypercalcaemia in surgical decision-making for elderly patients with mild cognitive deficiency.MethodsPatients with pHPT were included in a prospective observational study. A test panel including the Montreal Cognitive Assessment (MoCA) and validated tools for estimation of psychological status (Hospital Anxiety and Depression Scale, HADS), and muscle strength (timed-stands test, TST) was applied at baseline, after 4 weeks of calcimimetic treatment, and after parathyroidectomy. Mild cognitive impairment was defined by a MoCA score below 26. A longitudinal increase in MoCA score of at least 2 points 6 months after surgery was considered clinically meaningful.ResultsOf 110 patients who underwent testing, 35 aged 50 years or more were identified to have mild cognitive dysfunction, including 19 who were aged at least 70 years (median MoCA score 23, i.q.r. 21–24). Calcimimetic treatment resulted in normalization of calcium levels, and improvements in MoCA and HADS scores, and TST time. Normal MoCA scores (at least 26) were reached in 17 patients by 6 months after surgery, of whom 10 were aged 70 years or older. Long-term increase in MoCA score correlated with the decrease in ionized calcium concentration (r = –0.536, P = 0.022). Baseline calcium concentration and improvement in MoCA with calcimimetic treatment were identified as independent predictors of favourable outcome after parathyroidectomy.ConclusionMedical normalization of hypercalcaemia can aid in predicting outcome after parathyroidectomy.

Is statin related to conversion of mild cognitive impairment to dementia?

AbstractBackgroundAlthough randomized controlled trials have not confirmed cognitive impairing effects of statins, continuing evidence suggests statins have the ability to cause reversible cognitive impairment in some patients. Paradoxically, statins have also been shown to decrease risk of dementia, Alzheimer’s disease, and to improve cognitive impairment in some cases. However, randomized controlled trials have similarly failed to find the beneficial effect. We conducted evaluate the effect of statin on the conversion of mild cognitive impairment (MCI) to dementia in a Cohort of elderly individuals without functional and cognitive impaiment (NC) and with MCI patients.MethodCohort was reassessed annually by geriatricians and neuropsychologists for an average period of 3.01 ± 1.43 years. The effect of statin on cognition was evaluated when it was in use throughout the follow‐up period and, it was in use at any time during the follow‐up. Chi‐square and Fisher tests (categorical variables) and student t tests, ANOVA, Mann Whiney (continuous variables) were used.Results176 individuals were selected (53 CG, 111 with amnestic MCI ‐ aMCI‐ and 12 with non‐amnestic MCI ‐naMCI), aged 76.52 ± 7.27 years, 69% female and 3.61 ± 3.23 years of schooling. We observed conversion of aMCI to dementia in 27 participants (92.6% Alzheimer dementia), corresponding to a conversion rate of 24.3%. In the aMCI group, the remission rate was 13.5%. 51.1% of the sample received statin at some point during the follow‐up and 30.7% used it throughout the study. 98.8% of prescribed statins had moderate potency. Comparing stable MCI group throughout the study with the group which progressed to dementia, the group that used it any time during the follow‐up analysis showed a p‐value of 0.104, whereas the group that used it during the entire follow‐up showed a p‐value of 0.166. Comparing remission and conversion groups, the one that used statin any time during the follow‐up showed a p‐value of 0.542, patients who received statin during the entire follow‐up had a p‐value of 0.746.ConclusionStatins were not associated with conversion from aMCI to dementia, even when used throughout the entire follow‐up.

Pharmacological interventions for the treatment of delirium in critically ill adults.

Pharmacological interventions for the treatment of delirium in critically ill adults.

Reversal of Cognitive Impairment in gp120 Transgenic Mice by the Removal of the p75 Neurotrophin Receptor.

Activation of the p75 neurotrophin receptor (p75NTR), by the proneurotrophin brain-derived neurotrophic factor (proBDNF), triggers loss of synapses and promotes neuronal death. These pathological features are also caused by the human immunodeficiency virus-1 (HIV) envelope protein gp120, which increases the levels of proBDNF. To establish whether p75NTR plays a role in gp120-mediated neurite pruning, we exposed primary cultures of cortical neurons from p75NTR–/– mice to gp120. We found that the lack of p75NTR expression significantly reduced gp120-mediated neuronal cell death. To determine whether knocking down p75NTR is neuroprotective in vivo, we intercrossed gp120 transgenic (tg) mice with p75NTR heterozygous mice to obtain gp120tg mice lacking one or two p75NTR alleles. The removal of p75NTR alleles inhibited gp120-mediated decrease of excitatory synapses in the hippocampus, as measured by the levels of PSD95 and subunits of the N-methyl-D-Aspartate receptor in synaptosomes. Moreover, the deletion of only one copy of the p75NTR gene was sufficient to restore the cognitive impairment observed in gp120tg mice. Our data suggest that activation of p75NTR is one of the mechanisms crucial for the neurotoxic effect of gp120. These data indicate that p75NTR antagonists could provide an adjunct therapy against synaptic simplification caused by HIV.

Early detection of cognitive impairment in patients with insulinoma

Long-standing hypoglycemia can cause cognitive impairment, and whether recurrent severe hypoglycemia impacts cognitive function in patients with insulinoma has not been studied. This study focused on exploring the cognitive function in patients with insulinoma. A prospective study was conducted to assess cognitive function in patients with insulinoma by administering the Montreal Cognitive Assessment (MoCA) questionnaire between January 2016 and July 2017, and patients with cognitive impairment were followed up to undergo the MoCA test 1 year after surgery. The MoCA scores after surgery were compared with the scores before surgery, and the associations between cognitive impairment and relevant factors were further evaluated by multiple linear regression analysis. Eighteen out of thirty-four patients (53%) with insulinoma were screened positive for cognitive impairment as defined by a MoCA score <26. Performance in certain cognitive domains, including visuospatial and executive functions, delayed memory, attention, language, and abstraction, was significantly worse in patients with cognitive impairment. Multivariate analysis indicated that MoCA scores correlated significantly with tumor grade and years of education. Eight patients with cognitive impairment were lost to follow-up. The remaining ten patients with cognitive impairment showed improvements 1 year postoperatively, and seven patients recovered to normal cognitive function. Cognitive impairment was found in patients with insulinoma and was reversible in some patients 1 year after surgery. More studies are needed to explore the underlying mechanisms of the existence and reversibility of cognitive impairment in patients with insulinoma.