About this Research Topic
Cognitive dysfunction due to diabetes mellitus is gradually gaining attention. As early as 1965, Reske-Nielsen introduced the concept of diabetic encephalopathy (DE). In 2006, Mijnhout GS et al. found that the idea of DE did not express the impairment of cognitive function in diabetic patients, so they introduced the new term diabetes-associated cognitive decline (DACD). Up to the present, there is increasingly strong evidence of a link between diabetes mellitus DM) and cognitive dysfunction, ranging from mild cognitive decline with mild symptoms to mild cognitive impairment to more severe dementia.
The possible pathogenesis of DE involves an imbalance of pancreatic amyloid polypeptide homeostasis, Micro RNAs, macrophage autophagy, lipocalin Lipin1, advanced glycosylation end products (AGEs), oxidative stress, Tau protein hyperphosphorylation, and dysregulation of calcium homeostasis. In addition, some researchers have also found that the pathogenesis of DE may be related to synaptic plasticity, such as impaired synaptic plasticity and loss of synaptic proteins, which contribute to changes in the number and structural function of nerve cells, decreased cerebral blood flow, blood-brain barrier damage, and brain atrophy.
The possible pathogenesis of DE involves imbalance of pancreatic amyloid polypeptide homeostasis, Micro RNAs, macrophage autophagy, lipocalin Lipin1, advanced glycosylation end products (AGEs), oxidative stress, Tau protein hyperphosphorylation, and dysregulation of calcium homeostasis; thus, contributing to altered neuronal cell number and structural function, decreased cerebral blood flow, blood-brain barrier damage, and brain atrophy.
This research topic aims to highlight the frontiers and advances in DACD, covering but not limited to molecular biological mechanisms, diagnostic biomarkers, and therapeutic interventions, to add new insights into DE and enhance researchers' understanding of diabetic encephalopathy. Emphasis will be placed on the pathogenesis of DE, as this will help to identify more targeted therapeutic targets. For example, activating the mTOR/NF-κB signaling pathway plays a crucial role in DE, including loss of prominent proteins and impaired synaptic ultrastructure. And as another example, in DE, AGEs-induced oxidative stress leads to prominence deficits and poor cognition by mediating an increase in miR-34c targeting SYT1. Both the mTOR/NF-κB signaling pathway and miR-34c/SYT1 axis in the above two examples can be considered potential targets for preventing and treating DE. This provides new ideas for diagnosing and treating DE, which will help prevent, delay, or even suspend this irreversible disease.
We welcome all articles within the scope of this research topic that is acceptable according to journal policy: original research, reviews, protocols, editorial, etc., covering but not limited to, any one or more of the following topics:
- Disease mechanisms associated with DE include alterations in synaptic structure and function involving disease model organisms;
- Signaling pathways are involved in impairing synaptic plasticity in DACD;
- Imaging alterations in DE, emerging inflammatory biomarkers and therapeutic targets;
- T2DM and cognitive function, with particular reference to basic experimental research;
- Learn about the latest research advances in DE, global trends and hot spots, and more;
- Testing and understanding new cellular and animal models of DE;
- Treatment strategies.
The possible pathogenesis of DE involves an imbalance of pancreatic amyloid polypeptide homeostasis, Micro RNAs, macrophage autophagy, lipocalin Lipin1, advanced glycosylation end products (AGEs), oxidative stress, Tau protein hyperphosphorylation, and dysregulation of calcium homeostasis. In addition, some researchers have also found that the pathogenesis of DE may be related to synaptic plasticity, such as impaired synaptic plasticity and loss of synaptic proteins, which contribute to changes in the number and structural function of nerve cells, decreased cerebral blood flow, blood-brain barrier damage, and brain atrophy.
The possible pathogenesis of DE involves imbalance of pancreatic amyloid polypeptide homeostasis, Micro RNAs, macrophage autophagy, lipocalin Lipin1, advanced glycosylation end products (AGEs), oxidative stress, Tau protein hyperphosphorylation, and dysregulation of calcium homeostasis; thus, contributing to altered neuronal cell number and structural function, decreased cerebral blood flow, blood-brain barrier damage, and brain atrophy.
This research topic aims to highlight the frontiers and advances in DACD, covering but not limited to molecular biological mechanisms, diagnostic biomarkers, and therapeutic interventions, to add new insights into DE and enhance researchers' understanding of diabetic encephalopathy. Emphasis will be placed on the pathogenesis of DE, as this will help to identify more targeted therapeutic targets. For example, activating the mTOR/NF-κB signaling pathway plays a crucial role in DE, including loss of prominent proteins and impaired synaptic ultrastructure. And as another example, in DE, AGEs-induced oxidative stress leads to prominence deficits and poor cognition by mediating an increase in miR-34c targeting SYT1. Both the mTOR/NF-κB signaling pathway and miR-34c/SYT1 axis in the above two examples can be considered potential targets for preventing and treating DE. This provides new ideas for diagnosing and treating DE, which will help prevent, delay, or even suspend this irreversible disease.
We welcome all articles within the scope of this research topic that is acceptable according to journal policy: original research, reviews, protocols, editorial, etc., covering but not limited to, any one or more of the following topics:
- Disease mechanisms associated with DE include alterations in synaptic structure and function involving disease model organisms;
- Signaling pathways are involved in impairing synaptic plasticity in DACD;
- Imaging alterations in DE, emerging inflammatory biomarkers and therapeutic targets;
- T2DM and cognitive function, with particular reference to basic experimental research;
- Learn about the latest research advances in DE, global trends and hot spots, and more;
- Testing and understanding new cellular and animal models of DE;
- Treatment strategies.
Keywords: Diabetic encephalopathy, Diabetes-associated cognitive decline, Cognitive impairment, Dementia, Diabetes mellitus
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