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Last update 08 May 2025

Diabetic encephalopathy

Last update 08 May 2025

Basic Info

Synonyms

Diabetic encephalopathy, diabetic encephalopathy, 糖尿病性脳症

+ [1]

Introduction-

Drugs associated with Diabetic encephalopathy

PARIN5

Target

PAR-1

Mechanism

F2R antagonists

Active Org.

Tel-Aviv University [+1]

Originator Org.

Sheba Medical Center [+1]

Active Indication

Diabetic encephalopathy

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Diabetic encephalopathy

NCT02420470

/ RecruitingNot ApplicableIIT

The Early Warning System for the Central Nervous System Micro-structure Alterations During Early Diabetes Based on the Multi-mode MRIs

Diabetes( mainly type II diabetes )lead to the central nervous system (CNS) function impairment, especially the mild cognitive impairment that increased the risk of progression to dementia.The primary objectives are defined according to a hierarchical design: i) to tailor and apply multi-parametric, functional MRI techniques to identify cerebral abnormalities (cerebral biomarkers) in type 2 diabetes mellitus and prodromal diabetes mellitus ; ii) to assess whether these cerebral biomarkers are associated with cognitive decrements;iii) to follow up with the putative prediabetic condition patients to verify whether they can transform into diabetes.

Start Date01 Apr 2015

Sponsor / Collaborator

Tangdu Hospital

100 Clinical Results associated with Diabetic encephalopathy

100 Translational Medicine associated with Diabetic encephalopathy

0 Patents (Medical) associated with Diabetic encephalopathy

610

Literatures (Medical) associated with Diabetic encephalopathy

01 Aug 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Transcriptional profile and quantitative proteomics revealed NGF-p75NTR-associated synaptic plasticity and heterogeneity for diabetic encephalopathy and the potential role of CoQ10 for diabetic induced cognitive deficits in mice

Article

Author: Xiang, Qiong ; Lin, Hu ; Deng, Jing ; Li, Xian-Hui ; Tao, Jia-Sheng ; Liu, Li-Ni

BACKGROUNDDiabetic encephalopathy (DE) is one of the diabetes complications, which showing heterogeneous at different stage in course of disease. CoQ10 is well-known for its neuroprotection effects in cardiovascular system. However, whether CoQ10 could modulate synaptic plasticity in DE remains unknown. This study aims to explore the cellular and molecular characteristics of CoQ10 and its potential role in diabetic induced cognitive deficits (DICD).METHODSTMT-based quantitative proteomics was applied for investigating differentially expressed proteins (DEPs) among CoQ10 treated DICD, DICD and control (health) groups mice. Analysis of GO and KEGG pathway enrichment of DEPs among different groups. ScRNA-sequencing was applied for identifying heterogeneity among different groups; differentially expressed genes (DEGs), KEGG pathway enrichment were analyzed as well as Protein-protein interaction (PPI) networks were constructed. Western blotting was performed to validate the expressions of p75, BDNF in neurotrophin pathway and p-Akt in PI3K-Akt pathway, p-ERK as well as p-p38 in MAPK pathways among those groups.RESULTS29 upregulated and 13 downregulated DEPs (db vs control, p < 0.05); 46 upregulated and 11 downregulated DEPs (db + CoQ10 vs control, p < 0.05) and 8 upregulated and 7 downregulated DEPs (db vs db + CoQ10,p < 0.05) were identified totally. 35 KEGG pathways were enriched by DEPs between DICD and CoQ10 treated DICD, including neurotrophing signaling pathway that had a crucial role in development, plasticity, and repair of the nervous system; Zfp369 that could interact with p75 and was upregulated after CoQ10 treatment among the down regulated DEPs in DICD; Further, scRNA-seq was applied, and the integrated analysis showed type IC spiral ganglion neuron with marker gene expression in cluster2,3,5 and 9, which were involved in synaptic plasticity regulation such as axon guidance, positive regulation of neuron projection development, negative regulation of BDNF binding and negative regulation basement membrane and dendritic microtuble formation as well as axoneme assembly.CONCLUSIONSCoQ10 treatment was very important in neural plasticity of DICD mice. It was the pioneering study to investigate DICD- related and CoQ10 treated proteomic changes and the correlated heterogeneity alterations between DICD and control. And also, NGF-p75NTR signaling pathways were significantly involved in synaptic plasticity regulation. The findings supplied the cellular and molecular evidence to clarify the potential role of CoQ10 in DICD, and combined drugs for diabetic patients in clinic.

01 Jul 2025·Physiological Reviews

Neuropathological links between T2DM and LOAD: systematic review and meta-analysis

Review

Author: Turkheimer, Federico ; Kiecker, Clemens ; Hortobágyi, Tibor ; Lemche, Erwin

Recent decades have described parallel neuropathological mechanisms increasing the risk for developing late-onset Alzheimer’s dementia (LOAD) in type 2 diabetes mellitus (T2DM); however, still little is known of the role of diabetic encephalopathy and brain atrophy in LOAD. The aim of this systematic review is to provide a comprehensive view on diabetic encephalopathy/cerebral atrophy, taking into account neuroimaging data, neuropathology, metabolic and endocrine mechanisms, amyloid formation, brain perfusion impairments, neuroimmunology, and inflammasome activation. Key switches were identified, to further meta-analyze genomic candidate loci and epigenetic modifications. For the qualitative meta-analysis of genomic bases extracted, human linkage studies were examined; for epigenetic mechanisms, data from both human and animal studies are described. For the systematic review of pathophysiological mechanisms, 1,259 publications were evaluated and 93 gene loci extracted for candidate risk linkages. Sixty-six publications were evaluated for genomic association and descriptions of epigenomic modifications. Overall accumulated results highlight the insulin signaling system, vascular markers, inflammation and inflammasome pathways, amylin interactions, and glycosylation mechanisms. The protocol was registered with PROSPERO (ID: CRD42023440535).

01 Jul 2025·Experimental Neurology

DCI improves diabetic encephalopathy by modulating the BDNF/NF-κB/GSK-3β pathway

Article

Author: Gao, Linghuan ; Zhang, Haizhu ; Han, Xiao ; Zhang, Yuxin ; Zhu, Zhuoting ; Liu, Yirong ; Sun, Xinyu ; Wang, Gengyin ; Li, Shuang

Diabetic encephalopathy (DE) involves cognitive dysfunction and structural brain changes due to diabetes, with a complex pathogenesis and no specific treatments available. D-chiral inositol (DCI), a bioactive molecule from dietary sources, has hypoglycemic and anti-inflammatory effects, but its role in DE and the mechanisms involved are still unclear. This study focused on male db/db mice, treated continuously with D-chiral inositol (DCI) at doses of 35 and 70 mg/kg/day for 8 weeks. Cognitive function was evaluated using the Morris water maze test, while pathological changes in the hippocampus and cortex were assessed through hematoxylin-eosin (HE) staining and Nissl staining. Protein expression related to synapses, inflammation, apoptosis, and neurofibrillary tangles, as well as mRNA levels, were analyzed using qRT-PCR, immunohistochemistry, and Western blotting to evaluate DCI's effects on DE. The results showed that DCI improved learning and memory in db/db mice, reduced nuclear pyknosis and neuronal loss, normalized PSD95 and SYN protein levels, and modulated inflammatory and apoptosis-related factors in the hippocampus and cortex. Additionally, DCI increased the expression of BDNF, IκB-α, and p-GSK-3β (Ser9), while decreasing levels of NF-κB p65, p-GSK3 (α + β) (Y216 + Y279), P-Tau (Thr231), and P-Tau (Ser396). These findings suggest that DCI may alleviate DE by modulating the BDNF/NF-κB/GSK-3β signaling pathway.

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