Cognitive impairment in type 2 diabetes patients with and without diabetic peripheral neuropathy: a mismatch negativity study

Abstract

ObjectivesTo assess the cognitive impairment in patients with type 2 diabetes mellitus (T2DM) using mismatch negativity (MMN) and to explore the relationship between cognitive impairment and diabetic peripheral neuropathy (DPN).Methods Sixty-six T2DM patients and 40 healthy controls were included. For each participant, mini-mental state examination (MMSE) was applied to assess the general cognitive function and MMN was elicited. T2DM patients were divided into two subgroups: subgroup DPN−, patients without DPN; subgroup DPN+, patients with DPN. The MMSE scores, MMN amplitudes and latencies were compared between the T2DM group and the control group using univariate analysis of variance procedures, and also among the controls, subgroup DPN− and subgroup DPN+. Pearson's correlation coefficients (r) were used to analyze potential confounding clinical factors associated with MMN. Results T2DM patients had significantly lower MMSE scores compared with controls (23.25 ± 2.86 vs. 27.15 ± 1.83; P < 0.01), whereas those of the two subgroups were not significantly different. Both subgroup DPN+ and DPN− had longer latencies and lower amplitudes of MMN than the controls. The latencies of MMN were significantly longer in subgroup DPN+ compared with subgroup DPN−. The latency of MMN was positively correlated with the duration of the disease. Conclusion Cognitive decline exists in patients with T2DM irrespective of the presence of DPN. Patients with DPN may have more severe cognitive dysfunction than those without DPN. MMN may be a promising tool for evaluating cognitive function.

Towards prevention of diabetic peripheral neuropathy: clinical presentation, pathogenesis, and new treatments

“…56 Moreover, the risks between DPN and cognitive dysfunction are shared, and encompass both glucose and lipid centric mechanisms. 54,55 In clinical studies of patients with T1D and T2D, DPN is a risk for poorer cognitive function 57,58 and brain structural changes. 59 The possibility of shared or similar neurological damage in the periphery and centrally in diabetes is intriguing and the increasing burden of diabetes has implications for the future burden of dementia.…”

Altered N6-Methyladenosine Modification Patterns and Transcript Profiles Contributes to Cognitive Dysfunction in High-Fat Induced Diabetic Mice

“…m 6 A methylation is biased toward neuronal transcripts and is sensitive to neuronal activity [21]. In the hippocampus, m 6 A regulates several developmental and physiological processes, including neurogenesis, axonal growth, synaptic plasticity, circadian rhythms, cognitive function, and stress response [22]. With continuous progress in high-throughput sequencing technology, increasing attention to the m 6 A landscape has been focused on neoplastic and non-neoplastic diseases of the CNS.…”

Relationship between Cognitive Impairment and Depressive Symptoms with Somatosensory Functions in Diabetic and Non-Diabetic Older Adults and Its Impact on Quality of Life

“…In contrast, Manschot and co-workers [ 113 ] concluded that peripheral diabetic neuropathy, assessed by measuring pain, touch, and vibratory sensation, was not related to cognitive functions or brain abnormalities (in the form of white matter lesions and cortical and subcortical atrophy) when analyzed by magnetic resonance imaging. However, a recent study observed that CI was more common among diabetic patients regardless of the presence of peripheral neuropathy [ 49 ], although those with DM did have more severe cognitive dysfunctions. Accordingly, the pathophysiology of diabetic peripheral neuropathy and CI seem to share underlying mechanisms such as insulin dysregulation, inflammation, oxidative stress, and advanced glycation end products, as also suggested by some other authors [ 114 , 115 ].…”

“…Indeed, several studies have shown that type 2 DM is associated with CI in older adults [ 43 , 44 , 45 ], with the reported detection of reduced reasoning speed [ 46 , 47 ], memory [ 46 , 48 ], and executive functions in these patients [ 47 , 48 ]. Some work [ 49 , 50 ] has examined the relationships between peripheral and central nervous system damage in diabetic patients. However, the exploration of sensory functions has not yet been explored in depth, and many aspects of this field still require clarification.…”