Diabetes mellitus (DM) is one of the fastest growing diseases in terms of incidence worldwide and seriously affects cognitive function. The incidence rate of cognitive dysfunction is up to 13% in diabetes patients aged 65-74 and reaches 24% in those aged >75 years. The mechanisms and treatments of cognitive dysfunction associated with diabetes mellitus are complicated and varied. According to previous studies, hyperglycaemia mainly contributes to cognitive dysfunction through mechanisms involving inflammation, autophagy, the microbial-gut-brain axis, brain-derived neurotrophic factors and insulin resistance. Antidiabetic drugs such as metformin, liraglutide and empagliflozin and other drugs such as fingolimod and melatonin can alleviate cognitive dysfunction caused by diabetes. Self-management, indirect fasting and repetitive transverse magnetic stimulation can also ameliorate cognitive impairment. In this review, we discuss the mechanisms linking diabetes mellitus with cognitive dysfunction and propose a potential treatment for cognitive dysfunction related to diabetes mellitus.
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http://dx.doi.org/10.1055/a-2480-7826 | DOI Listing |
Metab Brain Dis
January 2025
Department of Pharmacy, the Second Affiliated Hospital of Shaoyang University, Shaoyang, Hunan, China.
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) plaques and the aggregation of tau protein, resulting in intense memory loss and dementia. Diabetes-associated cognitive dysfunction (DACD) is a complication of diabetes mellitus, which is associated with decreased cognitive function and impaired memory. A growing body of literature emphasize the involvement of microglia in AD and DACD.
View Article and Find Full Text PDFObjective: The aim of this study was to investigate the role of ferroptosis in the occurrence of postoperative cognitive dysfunction (POCD) using a mouse model and to elucidate whether electroacupuncture (EA) can improve POCD by suppressing ferroptosis via the transferrin receptor 1 (TFR1)-divalent metal transporter 1 (DMT1)-ferroportin (FPN) pathway.
Methods: The experiment involved three groups: the control group, the POCD group and the POCD + EA group. The POCD animal model was established using sevoflurane anesthesia and tibial fracture.
Background: Postoperative cognitive dysfunction (POCD) is a postoperative complication of the central nervous system, especially in elderly patients. Growing evidence shows a close relationship between the kidney and cognition. This study aimed to evaluate the relationship between the subsequent risk of POCD and indicators related to the kidney.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Neurology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Ave, Chicago, IL, 60611, USA.
Corticospinal motor neurons (CSMN), located in the motor cortex of the brain, are one of the key components of the motor neuron circuitry. They are in part responsible for the initiation and modulation of voluntary movement, and their degeneration is the hallmark for numerous diseases, such as amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegia, and primary lateral sclerosis. Cortical hyperexcitation followed by in-excitability suggests the early involvement of cortical dysfunction in ALS pathology.
View Article and Find Full Text PDFCell Death Dis
January 2025
Amsterdam UMC location Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands.
Aging of the brain vasculature plays a key role in the development of neurovascular and neurodegenerative diseases, thereby contributing to cognitive impairment. Among other factors, DNA damage strongly promotes cellular aging, however, the role of genomic instability in brain endothelial cells (EC) and its potential effect on brain homeostasis is still largely unclear. We here investigated how endothelial aging impacts blood-brain barrier (BBB) function by using excision repair cross complementation group 1 (ERCC1)-deficient human brain ECs and an EC-specific Ercc1 knock out (EC-KO) mouse model.
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