Consequences of diabetes mellitus on neuronal connectivity in limbic regions

Flores-Gómez, Alejandra Aketzalli; Gómez-Villalobos, Ma De Jesús; Flores, Gonzalo

doi:10.1002/syn.22082

Cited by 23 publications

(9 citation statements)

References 75 publications

(112 reference statements)

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“…At nanomolar concentrations, S100B has been indicated to have neurotrophic activity [24]. Previous studies have shown that the hippocampus is an important cognitive region of the brain, and cognitive dysfunction in diseases such as DM and AD has been found to be related to the hippocampus [27,28]. Nanomolar concentrations of S100B can promote hippocampal progenitor cell proliferation, neuronal differentiation and cognitive recovery [26].…”

Section: Discussionmentioning

confidence: 99%

Levels of serum S100B are associated with cognitive dysfunction in patients with type 2 diabetes

Liu

et al. 2020

Aging

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Objective: Previous studies have provided robust evidence that cognitive impairment exists in patients with type 2 diabetes. The predictive role of S100B in a variety of neurodegenerative diseases such as Alzheimer's disease, has been shown to be closely related to cognitive function. The purpose of this study was to investigate the correlation between serum S100B levels and cognitive function in type 2 diabetes patients. Results: The type 2 diabetes group scored lower than the healthy control group in all domains of cognitive function except language and attention, and the former group also had lower serum levels of S100B. Besides, serum S100B levels were lower in the type 2 diabetes patients with impaired cognition than in those with normal cognition. In addition, the moderate to severe cognitive impairment group had significantly lower levels than that in mild cognitive impairment group. After adjusting for confounding factors, serum S100B levels were positively correlated with cognitive function in type 2 diabetes patients. Conclusions: Serum S100B levels were positively correlated with cognitive function in type 2 diabetes patients with cognitive impairment. It is suggested that S100B may be involved in the occurrence and development of cognitive dysfunction in type 2 diabetes patients and play a protective role. Methods: The clinical data and biochemical indexes of ninety-six patients with type 2 diabetes and sixty-eight healthy subjects were collected. The levels of serum S100B were detected by enzyme-linked immunosorbent assay. Ninety-six type 2 diabetes patients were divided into a cognitive dysfunction group and a normal cognition group according to Mini-mental State Examination scores. To better understand the differences in various aspects of cognition, we used the Repeatable Battery for the Assessment of Neuropsychological Status scale for further evaluation. To study the relationship between serum S100B levels and cognitive impairment, the cognitive dysfunction group was divided into a mild cognitive impairment group and a moderate to severe cognitive impairment group for further study.

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Section: Discussionmentioning

confidence: 99%

Levels of serum S100B are associated with cognitive dysfunction in patients with type 2 diabetes

Liu

et al. 2020

Aging

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“…Considering that spine maturation, synaptic plasticity, and neuronal connectivity are reduced in metabolic imbalance conditions such as diabetes and obesity 60 , we assumed that exendin-4 may recover the neural structure and synaptic plasticity in the obese brain. Therefore, GLP-1 may be vital to the treatment of the diverse neuropathology caused by metabolic imbalance.…”

Section: Furthermore the Reduction Of Gsk-3β Activation Results In Tmentioning

confidence: 99%

Exendin-4 Improves Long-Term Potentiation and Neuronal Dendritic Growth in High-Fat Diet Mice and Neurons Under Metabolic Imbalance Conditions

Song¹,

Wang²,

Yoon³

et al. 2020

Preprint

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Metabolic syndrome, which increases the risk of obesity and type 2 diabetes, has emerged as a significant issue worldwide. Metabolic syndrome can occur due to diverse factors such as genetic background, lifestyle changes, food intake, and aging. Recent studies have highlighted the relationship between metabolic imbalance and neurological pathologies, such as synaptic dysfunction and memory loss. Glucagon-like peptide 1 (GLP-1) secreted from gut L-cells, and specific brain nuclei play multiple roles, including glucose metabolism, regulation of insulin sensitivity, inflammation control, synaptic plasticity improvement, and neuronal protection. Even though GLP-1 and GLP-1 receptor agonists (GLP-1RA) appear to have neuroprotective functions, the specific mechanisms of GLP-1 and GLP-1RA in brain function have remained unclear. Here, we investigated whether exendin-4 improves cognitive function and brain insulin resistance in metabolic imbalanced high-fat diet mice brain as a GLP-1RA, using electrophysiological experiments. Further, we identified the neuroprotective effect of exendin-4 in primary cultured hippocampal and cortical neurons under an in vitro metabolic imbalance condition, including neuronal structure improvement. This study provides significant findings on the effects of exendin-4 in synaptic plasticity, long-term potentiation (LTP), neuroinflammation, and neural structure. We suggest that GLP-1 may be vital to treating neuropathology caused by metabolic imbalance.

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“…The correlation between NfL and other biochemical parameter was unable to be made. The possible explanation might be the multiple comorbidities in ESRD patients, such as unmeasured uremic toxin contributing to neuroinflammation within the glial cells (Adesso et al, 2017) or the hyperglycemic status disturbing morphology of neuronal structure (Flores-Gómez et al, 2019). The higher percentage of diabetes mellitus in cognitive impairment group might influence the performance of NfL.…”

Section: The Role Of Nfl For Risk Assessment For Cognitive Impairmentmentioning

confidence: 99%

The Role of Plasma Neurofilament Light Protein for Assessing Cognitive Impairment in Patients With End-Stage Renal Disease

Hou

Huang

et al. 2021

Front. Aging Neurosci.

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Introduction: End-stage renal disease (ESRD) is defined as the irreversible loss of renal function, necessitating renal replacement therapy. Patients with ESRD tend to have more risk factors for cognitive impairment than the general population, including hypertension, accumulative uremic toxin, anemia, and old age. The association between these risk factors and the pathologic protein was lacking. Blood-based assays for detecting pathologic protein, such as amyloid beta (Aβ), total tau protein, and neurofilament light chain (NfL), have the advantages of being less invasive and more cost-effective for diagnosing patients with cognitive impairment. The aim of the study is to validate if the common neurologic biomarkers were different in ESRD patients and to differentiate if the specific biomarkers could correlate with specific correctable risk factors.Methods: In total, 67 participants aged >45 years were enrolled. The definition of ESRD was receiving maintenance hemodialysis for >3 months. Cognitive impairment was defined as a Mini-Mental State Examination score of <24. The participants were divided into groups for ESRD with and without cognitive impairment. The blood-based biomarkers (tau protein, Aβ1/40, Aβ1/42, and NfL) were analyzed through immunomagnetic reduction assay. Other biochemical and hematologic data were obtained simultaneously.Summary of results: The study enrolled 43 patients with ESRD who did not have cognitive impairment and 24 patients with ESRD who had cognitive impairment [Mini-Mental State Examination (MMSE): 27.60 ± 1.80 vs. 16.84 ± 6.40, p < 0.05]. Among the blood-based biomarkers, NfL was marginally higher in the ESRD with cognitive impairment group than in the ESRD without cognitive impairment group (10.41 ± 3.26 vs. 8.74 ± 2.81 pg/mL, p = 0.037). The concentrations of tau protein, amyloid β 1/42, and amyloid β 1/40 (p = 0.504, 0.393, and 0.952, respectively) were similar between the two groups. The area under the curve of NfL to distinguish cognitively impaired and unimpaired ESRD patients was 0.687 (95% confidence interval: 0.548–0.825, p = 0.034). There was no correlation between the concentration of NfL and MMSE among total population (r = −0.153, p = 0.277), patients with (r = 0.137, p = 0.583) or without cognitive impairment (r = 0.155, p = 0.333).Conclusion: Patients with ESRD who had cognitive impairment had marginally higher plasma NfL concentrations. NfL concentration was not correlated with the biochemical parameters, total MMSE among total population or individual groups with or without cognitive impairment. The concentrations of Aβ1/40, Aβ1/42, and tau were similar between the groups.

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Consequences of diabetes mellitus on neuronal connectivity in limbic regions

Cited by 23 publications

References 75 publications

Levels of serum S100B are associated with cognitive dysfunction in patients with type 2 diabetes

Levels of serum S100B are associated with cognitive dysfunction in patients with type 2 diabetes

Exendin-4 Improves Long-Term Potentiation and Neuronal Dendritic Growth in High-Fat Diet Mice and Neurons Under Metabolic Imbalance Conditions

The Role of Plasma Neurofilament Light Protein for Assessing Cognitive Impairment in Patients With End-Stage Renal Disease

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