&lt;p&gt;High Serum Neuron-Specific Enolase Level Is Associated with Mild Cognitive Impairment in Patients with Diabetic Retinopathy&lt;/p&gt;

Yu, Zi-Wei; Liu, Rong; Li, Xin; Wang, Ying; Fu, Yuhong; Li, Hui-Yao; Yuan, Yue; Gao, Xinyuan

doi:10.2147/dmso.s249126

Cited by 12 publications

(11 citation statements)

References 26 publications

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“…The correlation is in accordance with other data in the literature that showed overlap between anxiety and cognitive function [ 46 , 47 ]. The positive correlations of NSE with both short-term and medium-term neuro-cognitive outcome suggests that NSE can be used for selecting patients more prone to cognitive dysfunction, results supported by the data related to higher NSE values in other pathologies associated with the development of cognitive impairment [ 48 , 49 ].…”

Section: Discussionmentioning

confidence: 82%

Prediction of Neurocognitive Outcome after Moderate-Severe Traumatic Brain Injury Using Serum Neuron-Specific Enolase and S100 biomarkers

et al. 2020

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Seric biomarkers have been tested in a large number of studies on traumatic brain injuries (TBI) patients in order to predict severity, especially related to the short-term outcome. However, TBI patients have a high risk of developing long-term complications such as physical disability, cognitive impairment, psychiatric pathology, epilepsy, and others. The aim of this study was to assess the correlation between protein biomarkers S100 and neuron-specific enolase (NSE) and neurocognitive status at 10- and 90-days post-injury. Both biomarkers were tested in the first 4h and after 72h post-injury in 62 patients with moderate-severe TBI. The patients were evaluated by a series of neurocognitive tests: Early Rehabilitation Barthel Index (ERBI), Glasgow Outcome Scale-Extended (GOSE), The Mini-Mental State Examination (MMSE), Processing Speed Index (PSI), and Stroop Test, at 10 and 90 days post-injury and supplementary by the Hospital Anxiety and Depression Scale at 90 days. For evaluating the whole neurocognitive status instead of every scale separately, we used Structural Equation Modeling (SEM), while for anxiety and depressive symptoms, we used multiple regression analyses. SEM showed that NSE values at 4 hours were significant predictors of the cognitive status at 10 (p=0.034) and 90 days (p= 0.023). Also, there were found significant correlations between NSE at 4h and the anxiety level. This study demonstrated a significant correlation between NSE at 4h and short and medium-term neuropsychological outcomes, which recommends using this biomarker for selecting patients with a higher risk of cognitive dysfunction.

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Section: Discussionmentioning

confidence: 82%

Prediction of Neurocognitive Outcome after Moderate-Severe Traumatic Brain Injury Using Serum Neuron-Specific Enolase and S100 biomarkers

et al. 2020

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“…Once again, these findings were only observed in the Stressed group, underscoring the notion that chronic stress might trigger a detrimental cycle in the brain that impairs insulin signaling. The 3-year increases in serum NSE in this group might sensitively reflect injury of retinal neurovascular units as one of the main pathological mechanisms of early diabetic cognitive impairment [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

A Stress Syndrome Prototype Reflects Type 3 Diabetes and Ischemic Stroke Risk: The SABPA Study

Malan

Hamer

Känel

et al. 2021

Biology

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Type 3 diabetes (T3D) accurately reflects that dementia, e.g., Alzheimer’s disease, represents insulin resistance and neurodegeneration in the brain. Similar retinal microvascular changes were observed in Alzheimer’s and chronic stressed individuals. Hence, we aimed to show that chronic stress relates to T3D dementia signs and retinopathy, ultimately comprising a Stress syndrome prototype reflecting risk for T3D and stroke. A chronic stress and stroke risk phenotype (Stressed) score, independent of age, race or gender, was applied to stratify participants (N = 264; aged 44 ± 9 years) into high stress risk (Stressed, N = 159) and low stress risk (non-Stressed, N = 105) groups. We determined insulin resistance using the homeostatic model assessment (HOMA-IR), which is interchangeable with T3D, and dementia risk markers (cognitive executive functioning (cognitiveexe-func); telomere length; waist circumference (WC), neuronal glia injury; neuron-specific enolase/NSE, S100B). Retinopathy was determined in the mydriatic eye. The Stressed group had greater incidence of HOMA-IR in the upper quartile (≥5), larger WC, poorer cognitiveexe-func control, shorter telomeres, consistently raised neuronal glia injury, fewer retinal arteries, narrower arteries, wider veins and a larger optic cup/disc ratio (C/D) compared to the non-Stressed group. Furthermore, of the stroke risk markers, arterial narrowing was related to glaucoma risk with a greater C/D, whilst retinal vein widening was related to HOMA-IR, poor cognitiveexe-func control and neuronal glia injury (Adjusted R2 0.30; p ≤ 0.05). These associations were not evident in the non-Stressed group. Logistic regression associations between the Stressed phenotype and four dementia risk markers (cognitiveexe-func, telomere length, NSE and WC) comprised a Stress syndrome prototype (area under the curve 0.80; sensitivity/specificity 85%/58%; p ≤ 0.001). The Stress syndrome prototype reflected risk for HOMA-IR (odds ratio (OR) 7.72) and retinal glia ischemia (OR 1.27) and vein widening (OR 1.03). The Stressed phenotype was associated with neuronal glia injury and retinal ischemia, potentiating glaucoma risk. The detrimental effect of chronic stress exemplified a Stress syndrome prototype reflecting risk for type 3 diabetes, neurodegeneration and ischemic stroke.

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“…However, NSE levels are not 100% specific since extracranial tissues can also contribute to total serum levels if the patient suffers from severe multi-trauma or even haemolysis [51,52]. Although NSE levels correlate with mild cognitive impairment in conditions such as diabetic retinopathy and post-operative cognitive dysfunction after cardiac surgery [53,54], no relationship to NSE levels and cognitive decline have been reported in TBI [55].…”

Section: Discussionmentioning

confidence: 99%

Effects of Memantine in Patients with Traumatic Brain Injury: A Systematic Review

et al. 2021

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Traumatic brain injury (TBI) affects millions of people around the world and amongst other effects, causes cognitive decline, neurodegenerative disease and increased risk of seizures and sensory disturbances. Excitotoxicity and apoptosis occur after TBI and are mediated through the N-methyl-D-aspartate (NMDA)-type glutamate receptor. Memantine is effective in blocking excessive activity of NMDA-type glutamate receptors and reduces the progression of dementia and may have benefits after TBI. Here, we performed a systematic review of the literature to evaluate whether memantine is effective in improving outcomes, including cognitive function in patients with TBI. Our search yielded only 4 randomized control trials (RCTs) that compared the effects of memantine to placebos, standard treatment protocols or piracetam. A single RCT reported that serum neuron-specific enolase (NSE) levels were significantly reduced (p = 0.009) in the memantine compared to the control group, and this coincided with reported significant day-to-day improvements in Glasgow Coma Scale (GCS) for patients receiving memantine. The remaining RCTs investigated the effects of memantine on cognitive function using 26 standardized tests for assessing cognition function. One RCT reported significant improvements in cognitive function across all domains whilst the other two RCTs, reported that patients in the memantine group underperformed in all cognitive outcome measures. This review shows that despite laboratory and clinical evidence reporting reduced serum NSE and improved GCS, supporting the existence of the neuroprotective properties, there is a lack of reported evidence from RCTs to suggest that memantine directly leads to cognitive improvements in TBI patients.

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<p>High Serum Neuron-Specific Enolase Level Is Associated with Mild Cognitive Impairment in Patients with Diabetic Retinopathy</p>

Cited by 12 publications

References 26 publications

Prediction of Neurocognitive Outcome after Moderate-Severe Traumatic Brain Injury Using Serum Neuron-Specific Enolase and S100 biomarkers

Prediction of Neurocognitive Outcome after Moderate-Severe Traumatic Brain Injury Using Serum Neuron-Specific Enolase and S100 biomarkers

A Stress Syndrome Prototype Reflects Type 3 Diabetes and Ischemic Stroke Risk: The SABPA Study

Effects of Memantine in Patients with Traumatic Brain Injury: A Systematic Review

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