scholarly journals Brain Activation during Memory Encoding in Type 2 Diabetes Mellitus: A Discordant Twin Pair Study

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Amanda G. Wood ◽  
Jian Chen ◽  
Christopher Moran ◽  
Thanh Phan ◽  
Richard Beare ◽  
...  

Type 2 diabetes mellitus increases the risk of dementia and neuronal dysfunction may occur years before perceptible cognitive decline. We aimed to study the impact of type 2 diabetes on brain activation during memory encoding in middle-aged people, controlling for age, sex, genes, and early-shared environment. Twenty-two twin pairs discordant for type 2 diabetes mellitus (mean age 60.9 years) without neurological disease were recruited from the Australian Twin Registry (ATR) and underwent functional magnetic resonance imaging (fMRI) during a memory encoding task, cognitive tests, and structural MRI. Type 2 diabetes was associated with significantly reduced activation in left hemisphere temporoparietal regions including angular gyrus, supramarginal gyrus, and middle temporal gyrus and significantly increased activation in bilateral posteriorly distributed regions. These findings were present in the absence of within-pair differences in standard cognitive test scores, brain volumes, or vascular lesion load. Differences in activation were more pronounced among monozygotic (MZ) pairs, with MZ individuals with diabetes also displaying greater frontal activation. These results provide evidence for preclinical memory-related neuronal dysfunction in type 2 diabetes. They support the search for modifiable later-life environmental factors or epigenetic mechanisms linking type 2 diabetes and cognitive decline.

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jacqueline A. Bonds ◽  
Aashutosh Shetti ◽  
Terilyn K. L. Stephen ◽  
Marcelo G. Bonini ◽  
Richard D. Minshall ◽  
...  

Abstract Hippocampal neurogenesis plays an important role in learning and memory function throughout life. Declines in this process have been observed in both aging and Alzheimer’s disease (AD). Type 2 Diabetes mellitus (T2DM) is a disorder characterized by insulin resistance and impaired glucose metabolism. T2DM often results in cognitive decline in adults, and significantly increases the risk of AD development. The pathways underlying T2DM-induced cognitive deficits are not known. Some studies suggest that alterations in hippocampal neurogenesis may contribute to cognitive deterioration, however, the fate of neurogenesis in these studies is highly controversial. To address this problem, we utilized two models of T2DM: (1) obesity-independent MKR transgenic mice expressing a mutated form of the human insulin-like growth factor 1 receptor (IGF-1R) in skeletal muscle, and (2) Obesity-dependent db/db mice harboring a mutation in the leptin receptor. Our results show that both models of T2DM display compromised hippocampal neurogenesis. We show that the number of new neurons in the hippocampus of these mice is reduced. Clone formation capacity of neural progenitor cells isolated from the db/db mice is deficient. Expression of insulin receptor and epidermal growth factor receptor was reduced in hippocampal neurospheres isolated from db/db mice. Results from this study warrant further investigation into the mechanisms underlying decreased neurogenesis in T2DM and its link to the cognitive decline observed in this disorder.


2021 ◽  
Vol 15 ◽  
Author(s):  
Fei Qi ◽  
Dongsheng Zhang ◽  
Jie Gao ◽  
Min Tang ◽  
Man Wang ◽  
...  

Type 2 diabetes mellitus (T2DM) is related to a variety of cognitive impairments that may even progress to dementia. Studies have found the angular gyrus (AG) is a cross-modal integration hub that is involved in a variety of cognitive processes. However, few studies have focused on the patterns of resting-state functional connections (rsFCs) of the AG in patients with T2DM. This study explored the functional connection (FC) between the AG and the whole brain and the relationship between the FC and clinical/cognitive variables in patients with T2DM. 44 patients with T2DM and 43 sex-, age-, and education-matched healthy controls underwent resting-state fMRI and received neuropsychological assessments. Compared with the control group, the T2DM group showed abnormal rsFCs between the AG and multiple brain regions. The FC between the left AG and the left medial temporal lobe in the T2DM group was positively correlated with scores on the Montreal Cognitive Assessment, after a Bonferroni correction (r = 0.40, P = 0.009). Collectively, patients with T2DM have abnormal FCs between the AG and extensive brain regions that may be related to various cognitive processes.


Stroke ◽  
2017 ◽  
Vol 48 (9) ◽  
pp. 2368-2374 ◽  
Author(s):  
Einor Ben Assayag ◽  
Roy Eldor ◽  
Amos D. Korczyn ◽  
Efrat Kliper ◽  
Shani Shenhar-Tsarfaty ◽  
...  

2021 ◽  
Author(s):  
Jingyi Shen ◽  
Kaifeng Li ◽  
Huiyan Yu ◽  
Bingjie Ding ◽  
Rong Xiao ◽  
...  

Abstract In this study, we evaluated the cognitive function of 372 Chinese patients (214 males and 158 females; the average age was 57.09 ± 9.00 years) with type 2 diabetes mellitus (T2DM) by using the mini-mental state examination (MMSE) and the Montreal cognitive assessment (MoCA), with Plasma fatty acids measured by gas chromatography analysis and inflammatory cytokines determined by immune turbidimetric analysis and enzyme-linked immunosorbent assay (ELISA) to investigate whether there was a correlation between the plasma fatty acids, plasma inflammatory cytokine levels and cognitive test scores in Chinese patients with T2DM. We found the increasing of body mass index (BMI) might lead to cognitive impairment and induce inflammatory response. Higher saturated fatty acids (SFAs) levels in plasma were linked to cognitive decline, while higher monounsaturated fatty acids (MUFAs) intake might be a protective factor for cognitive function. In addition, most polyunsaturated fatty acids (PUFAs) levels stood out as having increasing trends that were positively correlated to cognitive function scores. In our study, we found higher SFAs led to higher proinflammatory factor levels. Apart from that, MUFAs and stearoyl-CoA desaturase-18 (SCD-18) were positively related to hypersensitive C-reactive protein (hs-CRP) (P<0.05; P<0.05; P<0.05). Meanwhile, our result also indicated that the increasing of C18:0 might reduce MoCA language skill scores by regulating plasma IL-10 levels. Plasma fatty acids could improve or damage cognitive function by regulating IL-10, which suggested plasma fatty acids could be evaluated as a potential indicator of cognitive function decline in T2DM.


2020 ◽  
Author(s):  
Katherine Samaras ◽  
Steve Makkar ◽  
John D. Crawford ◽  
Nicole A. Kochan ◽  
Wei Wen ◽  
...  

<b>Objective:</b> Type 2 diabetes mellitus (diabetes) is characterized by accelerated cognitive decline and higher dementia risk. Controversy exists regarding the impact of metformin which is associated with both increased and decreased dementia rates. The objective of this study was to determine the association of metformin-use with incident dementia and cognitive decline over 6 years in diabetes, compared to those not receiving metformin and those without diabetes. <p><b>Research</b> <b>Design and Methods</b>: Prospective observational study of N=1037 non-demented community-dwelling older participants aged 70-90 at baseline (the Sydney Memory and Ageing Study). Exclusion criteria were dementia, major neurological or psychiatric disease or progressive malignancy. Neuropsychological testing measured cognitive function every two years; a battery of tests measured executive function, memory, attention/speed, language and visuospatial function individually and to a construct of global cognition. Incident dementia was ascertained by a multidisciplinary panel. Total brain, hippocampal and parahippocampal volumes were measured by magnetic resonance at baseline and 2 years (n=526). Data were analyzed by linear mixed modeling, including the covariates of age, sex, education, body mass index, heart disease, hypertension, stroke, smoking and apolipoprotein Ee4 carriage. </p> <p><b>Results</b>: Of n=1037, 123 had diabetes; 67 received metformin (DM+MF) and were demographically similar to those not (DM-noMF) and participants without diabetes (no-DM). DM+MF had significantly slower global cognition and executive function decline compared to DM-noM. Incident dementia was significantly higher in DM-noMF compared to DM+MF (OR 5.29, 95%CI 1.17-23.88, p=0.05).</p> <p><b>Conclusions</b>: Older people with diabetes receiving metformin have slower cognitive decline and lower dementia risk. Large randomized studies in people with and without diabetes will determine whether these associations can be attributed to metformin. </p>


2021 ◽  
Author(s):  
Jingyi Shen ◽  
Kaifeng Li ◽  
Huiyan Yu ◽  
Bingjie Ding ◽  
Rong Xiao ◽  
...  

Abstract In this study, we evaluated the cognitive function of 372 Chinese patients (214 males and 158 females; the average age was 57.09 ± 9.00 years) with type 2 diabetes mellitus (T2DM) by using the mini-mental state examination (MMSE) and the Montreal cognitive assessment (MoCA), with Plasma fatty acids measured by gas chromatography analysis and inflammatory cytokines determined by immune turbidimetric analysis and enzyme-linked immunosorbent assay (ELISA) to investigate whether there was a correlation between the plasma fatty acids, plasma inflammatory cytokine levels and cognitive test scores in Chinese patients with T2DM. We found the increasing of body mass index (BMI) might lead to cognitive impairment and induce inflammatory response. Higher saturated fatty acids (SFAs) levels in plasma were linked to cognitive decline, while higher monounsaturated fatty acids (MUFAs) intake might be a protective factor for cognitive function. In addition, most polyunsaturated fatty acids (PUFAs) levels stood out as having increasing trends that were positively correlated to cognitive function scores. In our study, we found higher SFAs led to higher proinflammatory factor levels. Apart from that, MUFAs and stearoyl-CoA desaturase-18 (SCD-18) were positively related to hypersensitive C-reactive protein (hs-CRP) (P<0.05; P<0.05; P<0.05). Meanwhile, our result also indicated that the increasing of C18:0 might reduce MoCA language skill scores by regulating plasma IL-10 levels. Plasma fatty acids could improve or damage cognitive function by regulating IL-10, which suggested plasma fatty acids could be evaluated as a potential indicator of cognitive function decline in T2DM.


Sign in / Sign up

Export Citation Format

Share Document