ArticleThe Journal of biological chemistry2013
Diabetes-induced central neuritic dystrophy and cognitive deficits are associated with the formation of oligomeric reticulon-3 via oxidative stress.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 38 citations in OpenAlex.
- BMECs Ameliorate High Glucose-Induced Morphological Aberrations and Synaptic Dysfunction via VEGF-Mediated Modulation of Glucose Uptake in Cortical Neurons.Cellular and molecular neurobiology · 2023Article
- Inhibition of the Proteasome Regulator PA28 Aggravates Oxidized Protein Overload in the Diabetic Rat Brain.Cellular and molecular neurobiology · 2023Article
- Molecular alteration of the proteasome contributes to AD-like pathology in the brain of HFD-STZ diabetic rats.Metabolic brain disease · 2023Article
- Sex-specific metabolic alterations in the type 1 diabetic brain of mice revealed by an integrated method of metabolomics and mixed-model.Computational and structural biotechnology journal · 2020Article
- Axonal Endoplasmic Reticulum Dynamics and Its Roles in Neurodegeneration.Frontiers in neuroscience · 2020Review
- A New Vision for Therapeutic Hypothermia in the Era of Targeted Temperature Management: A Speculative Synthesis.Therapeutic hypothermia and temperature management · 2019Review
- Identification of rare RTN3 variants in Alzheimer's disease in Han Chinese.Human genetics · 2018Article
- MicroRNA-146a: A Comprehensive Indicator of Inflammation and Oxidative Stress Status Induced in the Brain of Chronic T2DM Rats.Frontiers in pharmacology · 2018Article
- Sevoflurane Induces Exaggerated and Persistent Cognitive Decline in a Type II Diabetic Rat Model by Aggregating Hippocampal Inflammation.Frontiers in pharmacology · 2017Article
- Hyperactivation of working memory-related brain circuits in newly diagnosed middle-aged type 2 diabetics.Acta diabetologica · 2015Article
- Astaxanthin improves cognitive deficits from oxidative stress, nitric oxide synthase and inflammation through upregulation of PI3K/Akt in diabetes rat.International journal of clinical and experimental pathology · 2015Article
- The role of reticulons in neurodegenerative diseases.Neuromolecular medicine · 2014Review
- Can BACE1 inhibition mitigate early axonal pathology in neurological diseases?Journal of Alzheimer's disease : JAD · 2014Review
- Increased expression of reticulon 3 in neurons leads to reduced axonal transport of β site amyloid precursor protein-cleaving enzyme 1.The Journal of biological chemistry · 2013Article
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7 authors at 4 institutions in 2 countries.
Funding
Abstract
Diabetes is a high risk factor to dementia. To investigate the molecular mechanism of diabetic dementia, we induced type 2 diabetes in rats and examined potential changes in their cognitive functions and the neural morphology of the brains. We found that the diabetic rats with an impairment of spatial learning and memory showed the occurrence of RTN3-immunoreactive dystrophic neurites in the cortex. Biochemical examinations revealed the increase of a high molecular weight form of RTN3 (HW-RTN3) in diabetic brains. The corresponding decrease of monomeric RTN3 was correlated with the reduction of its inhibitory effects on the activity of β-secretase (BACE1), a key enzyme for generation of β-amyloid peptides. The results from immunoprecipitation combined with protein carbonyl detection showed that carbonylated RTN3 was significantly higher in cortical tissues of diabetic rats compared with control rats, indicating that diabetes-induced oxidative stress led to RTN3 oxidative damage. In neuroblastoma SH-SY5Y cells, high glucose and/or H2O2 treatment significantly increased the amounts of carbonylated proteins and HW-RTN3, whereas monomeric RTN3 was reduced. Hence, we conclude that diabetes-induced cognitive deficits and central neuritic dystrophy are correlated with the formation of aggregated RTN3 via oxidative stress. We provided the first evidence that oxidative damage caused the formation of toxic RTN3 aggregates, which participated in the pathogenesis of central neuritic dystrophy in diabetic brain. Present findings may offer a new therapeutic strategy to prevent or reduce diabetic dementia.
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