Cognitive Dysfunctions in Middle-Aged Type 2 Diabetic Patients and Neuroimaging Correlations: A Cross-Sectional Study

García‐Casares, Natalia; Jorge, Ricardo E.; García-Arnés, Juan Antonio; Ación, Laura; Berthier, Marcelo L.; Gonzalez‐Alegre, Pedro; Nabrozidis, Alejandro; Gutiérrez, Antonio; Ariza, María José; Rioja, José; González-Santos, Pedro

doi:10.3233/jad-140702

Cited by 70 publications

(58 citation statements)

References 35 publications

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“…Impaired executive function and memory is correlated with reduced gray matter density and reduced glucose metabolism in the orbital and prefrontal cortex, temporal cortex (middle gyrus, parahippocampus, and uncus), and cerebellar regions [27]. While both T1DM [28] and T2DM [28] are associated with impaired cognition, the current data suggests a stronger association with T2DM.…”

Section: Clinical Effects Of Diabetes On Cognitionmentioning

confidence: 86%

Diabetes and Cognitive Impairment

et al. 2016

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Both type 1 (T1DM) and type 2 diabetes mellitus (T2DM) have been associated with reduced performance on multiple domains of cognitive function and with evidence of abnormal structural and functional brain magnetic resonance imaging (MRI). Cognitive deficits may occur at the very earliest stages of diabetes and are further exacerbated by the metabolic syndrome. The duration of diabetes and glycemic control may have an impact on the type and severity of cognitive impairment, but as yet we cannot predict who is at greatest risk of developing cognitive impairment. The patho-physiology of cognitive impairment is multifactorial, although dysfunction in each interconnecting pathway ultimately leads to discordance in metabolic signaling. The pathophysiology includes defects in insulin signaling, autonomic function, neuroinflammatory pathways, mitochondrial (Mt) metabolism, the sirtuin-peroxisome proliferator-activated receptor-gamma co-activator 1α (SIRT-PGC-1α) axis, and Tau signaling. Several promising therapies have been identified in pre-clinical studies, but remain to be validated in clinical trials.

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Section: Clinical Effects Of Diabetes On Cognitionmentioning

confidence: 86%

Diabetes and Cognitive Impairment

et al. 2016

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“…[32] Other studies of diabetes also found significant reductions in the GMV of the STG and MTG. [9,33] Another study showed that the GMV alterations in the MTG may predict mild cognitive impairment in type 2 diabetic patients. [34] Our findings in the STG and MTG may be associated with glucose dysregulation in prediabetes.…”

Section: Discussionmentioning

confidence: 99%

Gray matter alterations and correlation of nutritional intake with the gray matter volume in prediabetes

Hou

Lai

et al. 2016

Medicine

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The neurophysiology of prediabetes plays an important role in preventive medicine. The dysregulation of glucose metabolism is likely linked to changes in neuron-related gray matter. Therefore, we designed this study to investigate gray matter alterations in medication-naive prediabetic patients. We expected to find alterations in the gray matter of prediabetic patients.A total of 64 prediabetic patients and 54 controls were enrolled. All subjects received T1 scans using a 3-T magnetic resonance imaging machine. Subjects also completed nutritional intake records at the 24-hour and 3-day time points to determine their carbohydrate, protein, fat, and total calorie intake. We utilized optimized voxel-based morphometry to estimate the gray matter differences between the patients and controls. In addition, the preprandial serum glucose level and the carbohydrate, protein, fat, and total calorie intake levels were tested to determine whether these parameters were correlated with the gray matter volume.Prediabetic patients had lower gray matter volumes than controls in the right anterior cingulate gyrus, right posterior cingulate gyrus, left insula, left super temporal gyrus, and left middle temporal gyrus (corrected P < 0.05; voxel threshold: 33). Gray matter volume in the right anterior cingulate was also negatively correlated with the preprandial serum glucose level gyrus in a voxel-dependent manner (r = –0.501; 2-tailed P = 0.001).The cingulo-temporal and insula gray matter alterations may be associated with the glucose dysregulation in prediabetic patients.

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“…A longitudinal neuropsychological study has convincingly shown that patients with damage to PFC exhibit disorders in the higher cognitive functions (Cohen, 2000). Clinical research indicated that the terrible executive function and memory lesion in T2DM correlated predominantly with reduced glucose metabolism in the mPFC and orbital, temporal, and cerebellum regions (Garcia-Casares et al, 2014). Some studies suggested the memory dysfunction occurred in T2DM patients during acute hyperglycemia (Cox et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Berberine Ameliorates Diabetes-Associated Cognitive Decline through Modulation of Aberrant Inflammation Response and Insulin Signaling Pathway in DM Rats

Chen

et al. 2017

Front. Pharmacol.

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Background: Memory-impairment was one of the common characteristics in patients with diabetes mellitus. The release of chronic inflammation mediators and insulin resistance in diabetic brain gave rise to the generation of toxic factor Aβ42 which was the marker of Alzheimer’s disease. In addition, the impairment of memory in diabetes mellitus was also correlated predominantly with uptake/metabolism of glucose in medial prefrontal cortex (mPFC). Previously, anti-inflammation and hypoglycemic effects of berberine (BBr) have been described in peripheral tissues. For better understanding the effects of BBr on cognitive action in diabetics, we investigated the functions of BBr involved in anti-inflammation and ameliorating insulin resistance in prefrontal cortex of diabetic rats.Methods: Intragastric administration of BBr (187.5 mg/Kg/d) was used in diabetic rats. Fear-condition assay was applied for cognitive assessment, and relative protein expressions were detected by western-blot. The glucose uptake in prefrontal cortex of diabetic rats was tested by Positron-Emission Tomography imaging. The levels of inflammation mediators were determined by commercial ELISA kits.Results: The inflammation mediator release and insulin resistance in the mPFC of diabetic rats was inhibited by BBr. The activation of PI3K/Akt/mTOR and MAPK signaling pathway, as well as two novel isoforms PKCη and PKC𝜀 and the translocation of NF-κB in neuron were also down-regulated by BBr; furthermore, the neuron specific glucose transporter GLUT3 was remarkably augmented by 2–3 times when compared with diabetic group; meanwhile, BBr also promoted glucose uptake in the brain. Additionally BBr decreased the expressions of amyloid precursor protein and BACE-1, and the production of oligomeric Aβ42. Finally, it accelerates the reinforcement of the information and ameliorates cognitive impairment.Conclusion: BBr inhibited the activation of inflammation pathway and insulin resistance in the mPFC of diabetic rats. Finally, it improved the lesion of cognition in diabetic rats.

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Cognitive Dysfunctions in Middle-Aged Type 2 Diabetic Patients and Neuroimaging Correlations: A Cross-Sectional Study

Abstract: T2DM subjects presented cognitive dysfunctions compared with controls. Clinical-neuroimaging correlations corresponded to brain changes (reduced gray matter density and glucose metabolism) mainly in fronto-temporal areas.

Cited by 70 publications

References 35 publications

Diabetes and Cognitive Impairment

Diabetes and Cognitive Impairment

Gray matter alterations and correlation of nutritional intake with the gray matter volume in prediabetes

Berberine Ameliorates Diabetes-Associated Cognitive Decline through Modulation of Aberrant Inflammation Response and Insulin Signaling Pathway in DM Rats

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