scholarly journals Changes in cognitive function in patients with diabetes mellitus

2012 ◽  
Vol 153 (9) ◽  
pp. 323-329 ◽  
Author(s):  
Barbara Szémán ◽  
Géza Nagy ◽  
Tímea Varga ◽  
Anna Veres-Székely ◽  
Mária Sasvári ◽  
...  

Patients with diabetes are approximately 1.5 times more likely to experience cognitive decline than individuals without diabetes mellitus. Most of the data suggest that patients with diabetes have reduced performance in numerous domains of cognitive function. In patients with type 1 diabetes, specific and global deficits involving speed of psychomotor efficiency, information processing, mental flexibility, attention, and visual perception seem to be present, while in patients with type 2 diabetes an increase in memory deficits, a reduction in psychomotor speed, and reduced frontal lobe (executive) functions have been found. The complex pathophysiology of changes in the central nervous system in diabetes has not yet been fully elucidated. It is important to consider the patient’s age at the onset of diabetes, the glycemic control status, and the presence of diabetic complications. Neurological consequences of diabetes appear parallel to those observed in the aging brain. Neuroimaging studies highlight several structural cerebral changes, cortical and subcortical atrophy, beside increased leukoaraiosis that occurs in association with diabetes. There is supporting evidence from many hypotheses to explain the pathophysiology of cognitive decline associated with diabetes. The main hypotheses pointing to the potential, implied mechanisms involve hyperglycemia, hypoglycemia, microvascular disease, insulin resistance, hyperinsulinism, hyperphosphorylation of tau protein, and amyloid-β deposition. Orv. Hetil., 2012, 153, 323–329.

2021 ◽  
pp. 1-9
Author(s):  
Gihwan Byeon ◽  
Min Soo Byun ◽  
Dahyun Yi ◽  
Jun Ho Lee ◽  
So Yeon Jeon ◽  
...  

Background: Both elevated blood homocysteine and diabetes mellitus (DM) are related to cognitive impairments or dementia. A previous study also demonstrated that the association between homocysteine and cognitive decline was much stronger in individuals with DM than in those without DM. Objective: This study aimed to examine the interactive effect of blood homocysteine and DM on brain pathological changes including brain atrophy, amyloid-β and tau deposition, and small vessel disease (SVD) related to cognitive impairments. Methods: A total of 430 non-demented older adults underwent comprehensive clinical assessment, measurement of serum homocysteine level, [11C] Pittsburgh Compound B (PiB) PET, [18F] AV-1451 PET, and brain MRI. Results: The interactive effect of homocysteine with the presence of DM on brain atrophy, especially in aging-related brain regions, was significant. Higher homocysteine concentration was associated with more prominent brain atrophy in individuals with DM, but not in those without DM. In contrast, interaction effect of homocysteine and DM was found neither on Alzheimer’s disease (AD) pathologies, including amyloid-β and tau deposition, nor white matter hyperintensity volume as a measure of SVD. Conclusion: The present findings suggest that high blood homocysteine level and DM synergistically aggravate brain damage independently of AD and cerebrovascular disease. With regard to preventing dementia or cognitive decline in older adults, these results support the importance of strictly controlling blood glucose in individuals with hyperhomocysteinemia and lowering blood homocysteine level in those with DM.


2021 ◽  
pp. 209-219
Author(s):  
Susy Puspasari ◽  
Endar Andrianto

Cognitive decline in diabetes mellitus is not fully understood, though is generally ascribed to blood sugar levels exceeding normal (hyperglycemia), hypoglycemia conditions and insulin resistance. Cognitive function consists of aspects of memory, attention, executive function, perception, language, and psychomotor functions which affect the decline in cognitive function, especially in people with Diabetes Mellitus. This study aims to summarize the results of research on cognitive function in people with Diabetes Mellitus. The research method used was a literature review with an assessment using JBI critical appraisal tools. Articles were sourced via the PubMed database and Google Scholar using the search term ‘Cognitive Function AND Diabetes Mellitus’. The inclusion criteria were studies with quantitative design, full text, a population comprised of patients with Diabetes Mellitus, written in Indonesian or English. Six articles were reviewed, all the results state that patients with Diabetes Mellitus experienced a decrease in cognitive function, especially in the Executive Function, Visuospatial, and the Memory Domains.   Keywords: Cognitive function, Diabetes mellitus, Literature review


Oncotarget ◽  
2017 ◽  
Vol 9 (7) ◽  
pp. 7710-7726 ◽  
Author(s):  
Xue Zhao ◽  
Qing Han ◽  
You Lv ◽  
Lin Sun ◽  
Xiaokun Gang ◽  
...  

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 1099-1099
Author(s):  
Chen Nemin ◽  
Christina Caruso ◽  
Alvaro Alonso ◽  
Vimal K. Derebail ◽  
Abhijit V Kshirsagar ◽  
...  

Abstract Background: The prevalence of cerebral small vessel disease (CSVD) and its associated complication of cognitive decline is significantly higher amongst African Americans than non-Hispanic Whites. Sickle cell anemia or sickle cell disease has been associated with a 30-45% increased prevalence of CSVD which presents as silent cerebral infarcts and impaired cognitive function. However, the association between sickle cell trait (heterozygosity for the sickle cell mutation) and cognitive decline or dementia has not been reported. Hypothesis: African Americans with SCT will have a significantly higher incidence and prevalence of cognitive impairment and dementia compared to those without SCT. Methods: We studied African Americans participants enrolled in the community-based prospective Atherosclerosis Risk in Communities (ARIC) study. SCT genotype status was determined using Taqman® genotyping from blood samples collected at baseline. Data from cognitive assessments at visits 2, 4 and 5, and an MRI performed at visit 5 were used for analysis. Using linear regression models for visit 2 cognitive measures and visit 5 brain MRI outcomes, a generalized estimating equation (GEE) for cognitive change, and Cox models for the incidence of dementia, we determined whether SCT was associated with a higher risk for cognitive dysfunction, global and regional brain volumes, and dementia. Results: Distribution of traditional risk factors for cognitive decline were not significantly different between participants with SCT (N = 176) and those without SCT (N = 2,532). In multivariable, cross-sectional analyses of 2,708 participants, those participants with SCT compared to those without SCT did not show a statistically significant difference in the global or domain-specific cognitive function scores at baseline. Participants with SCT did not experience a faster 20-year cognitive decline compared to participants without SCT. Also, participants with SCT had larger parietal cortical volume (100.5 cm3 vs. 97.9 cm3, diff. = 2.67 (0.24, 5.11) cm3, p = 0.03), and lower incidence of dementia (HR = 0.63 95% CI = 0.38, 1.05) compared to those without SCT. Participants with a co-inheritance of the apolipoprotein E (APOE) ε4 risk allele and SCT (N = 63) had worse scores on the digit symbol substitution test (DSST) at baseline (z-score = -0.08 (-0.26, 0.09), Pinteraction = 0.05) and over time (z-score = -0.12 (-0.38, 0.14), Pinteraction = 0.04), compared to those with the APOE ε4 risk allele who do not have SCT (N = 113). SCT was associated with 2-fold increased risk of dementia among participants with diabetes mellitus and a 55% reduction in risk of dementia among those without diabetes mellitus (Pinteraction = 0.01). Conclusions: SCT was not an independent risk factor for prevalent or incident cognitive decline, but it could potentially interact with and modify other risk factors for dementia and cognitive dysfunction. Disclosures Key: UniQure BV: Research Funding.


Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Li Zhang ◽  
Michael Chopp ◽  
Chao Li ◽  
Quan Jiang ◽  
Guang Liang Ding ◽  
...  

Introduction: Diabetes mellitus (DM) is associated with cognitive decline and dementia in the elderly. The glymphatic system mediates clearance of the interstitial solutes in the brain by exchange of cerebrospinal and interstitial fluid (CSF and ISF). We recently demonstrated that DM in aged rat induces impairment of the glymphatic system and cognitive decline. Exosomes, membrane vesicles, mediate intercellular communication by transferring their cargo into recipient cells. The present study investigated whether cerebral endothelial exosomes (CEE) ameliorate glymphatic system impairment and improve cognitive function in aged DM rats. Methods and Results: DM was induced in male Wistar rats (13 months, n=48) by injection of nicotinamide and streptozotocin. Two months after DM, rats were treated with CEE (1x10 11 exosomes/rat, IV) twice a week for 4 weeks. Age matched DM and non-DM rats were used as controls. CEE were harvested from the cultured cerebral endothelial cells of health young adult rats. Exchanges of CSF and ISF were measured by intracisternal injection of fluorescent tracer, Texas Red-dextran (TR, 3kD). Confocal microscopic analysis of brain slices revealed a progressive slowdown of ISF clearance in the hippocampi, assessed by retention of TR starting at 2.5 fold at 2M (13±5 vs 5±3% of area) and increasing to 4 fold at 4M (21±4 vs 5±2%) of DM. Paravascular amyloid β (Aβ) accumulation was only detected at 4M of DM. The CEE treatment significantly (p<0.05) reduced TR retention (10±4%) at 4M of DM and also decreased Aβ accumulation (2±1 vs 6±2/mm 2 ) and parenchymal fibrin deposition (9±5 vs 23±5/mm 2 ) compared to untreated DM rats. Moreover, the CEE treatment significantly improved hippocampal related learning and memory measured by the Morris Water Maze and odor-based novelty recognition for olfactory memory, without altering the glucose level. In vitro, cerebral endothelial cells isolated from 2M DM rats exhibited substantial dysfunction as measured by capillary-like tube formation and cell migration, whereas incubation with the CEE substantially reversed endothelial dysfunction. Conclusions: The CEE treatment reduces DM-induced glymphatic and cerebral endothelial dysfunctions, leading to improvement of cognitive function in aged DM rats.


2007 ◽  
Vol 4 (2_suppl) ◽  
pp. S7-S11 ◽  
Author(s):  
Michel P Hermans

Before a patient develops overt type 2 diabetes mellitus, there is typically a prolonged period of patho-physiological change. In the common form of type 2 diabetes mellitus, there are years of insulin resistance, initially compensated by increased beta cell function, then impaired glucose tolerance develops, and finally type 2 diabetes. We know from studies such as the United Kingdom Prospective Diabetes Study (UKPDS) and the Belfast study that loss of beta cell function and insulin resistance are usually relentless.1, 2 Thus, therapy to reduce blood glucose has to be gradually increased with time for patients with diabetes. What is less well known is that every person has a different slope for beta cell function loss which intersects with insulin resistance.


2012 ◽  
Vol 3 ◽  
pp. S142 ◽  
Author(s):  
G.I. Prada ◽  
I.D. Alexa ◽  
I.G. Fita ◽  
M. Gaiculescu ◽  
R. Nacu ◽  
...  

2015 ◽  
Vol 14 (3) ◽  
pp. 329-340 ◽  
Author(s):  
Paula S Koekkoek ◽  
L Jaap Kappelle ◽  
Esther van den Berg ◽  
Guy E H M Rutten ◽  
Geert Jan Biessels

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