Background: Gestational diabetes mellitus (GDM) is a prevalent metabolic disorder that disrupts fetal central nervous system (CNS) development. This study investigates the effects of maternal diabetes on hippocampal structure and autophagy-related mechanisms in neonatal rats, focusing on the PI3K/mTOR signaling pathway.
Methods: Forty female Wistar rats were divided into three groups: control (CON), diabetic (STZ-D), and insulin-treated diabetic (STZ-INS).
Many systemic and ocular diseases cause macular edema (ME). Macular edema is seen in two primary forms; the first is diffuse thickening of the macula, and the other is a macula with a distinct petaloid (cloverleaf) appearance called cystoid macular edema. Macular edema has a known role in the reduction of visual equity, and many options have been proposed for the reversal of this condition.
View Article and Find Full Text PDFJ Lasers Med Sci
July 2022
Multiple sclerosis (MS) is one of the autoimmune and chronic diseases of the central nervous system; this disease occurs more frequently in young people and women and leads to neurological symptoms. Oxidative stress, inflammatory processes, and oligodendrocyte dysfunction have a pivotal role in the pathophysiology of this disease. Nowadays it is reported that photobiomodulation (PBM) as a non-invasive treatment has neuroprotective potential, but the exact mechanisms are not understood.
View Article and Find Full Text PDFMesenchymal stem cells (MSCs) and mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have been regarded as the beneficial and available tools to treat various hereditary, multifactorial, acute, and chronic diseases. Mesenchymal stem cells can be extracted from numerous sources for clinical purposes while oral cavity-derived mesenchymal stem cells seem to be more effective in neuroregeneration than other sources due to their similar embryonic origins to neuronal tissues. In various studies and different neurodegenerative diseases (NDs), oral cavity mesenchymal stem cells have been applied to prove their promising capacities in disease improvement.
View Article and Find Full Text PDFFollowing severe Spinal Cord Injury (SCI), regeneration is inadequate, and functional recovery is incomplete. The occurrence of oxidative stress and the spread of inflammation play a crucial role in the failure to regenerate the injury site. In this way, we explored the neuroprotective effects of PhotoBioModulation (PBM), as the main factor in controlling these two destructive factors, on SCI.
View Article and Find Full Text PDFSpinal cord injury (SCI) can cause various symptoms, including pain, complete or incomplete loss of autonomic, sensory, motor and functions inferior to the site of the damage. Despite wondrous advances in medicine, treating spinal cord injuries remains a thorny issue yet. Recently, the control of inflammatory processes after damage to the nervous system has been noticed as a promising therapeutic target.
View Article and Find Full Text PDFJ Lasers Med Sci
October 2020
Damage to the spinal cord is a central nervous system disorder that results in direct damage to neural cells (axons, cell bodies) and glia, followed by autonomic, motor and sensory impairments. Inflammatory response after this injury can contribute to secondary tissue damage that leads to further behavioral and functional disorders. Inflammation is a complex process, which occurs after an injury.
View Article and Find Full Text PDFJ Pediatr Neurosci
January 2017
There is increasing evidence that maternal diabetes mellitus during the pregnancy is associated with a higher risk of neurodevelopmental and neurofunctional anomalies including motor dysfunctions, learning deficits, and behavioral problems in offspring. The cerebellum is a part of the brain that has long been recognized as a center of movement balance and motor coordination. Moreover, recent studies in humans and animals have also implicated the cerebellum in cognitive processing, sensory discrimination, attention, and learning and memory.
View Article and Find Full Text PDFBackground: L-arginine has been recently investigated and proposed to reduce neurological damage after various experimental models of neuronal cellular damage. In this study, we aim to evaluate the beneficial effects of L-arginine administration on the numerical density of dark neurons (DNs) in the substantia nigra pars compacta (SNc) of Balb/c mice subjected to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration.
Materials And Methods: Male Balb/c mice were randomly divided into 4 groups (n = 7 each): MPTP only; saline only (control); MPTP + L-arginine; and L-arginine only.
There is sufficient evidence that diabetes during pregnancy is associated with a higher risk of neurodevelopmental anomalies including learning deficits, behavioral problems and motor dysfunctions in the offspring. Synaptophysin (SYP) is an integral membrane protein of synaptic vesicles and is considered as a marker for synaptogenesis and synaptic density. This study aimed to examine the effects of maternal diabetes in pregnancy on the expression and localization of SYP in the developing rat cerebellum.
View Article and Find Full Text PDFDiabetes during pregnancy is associated with the deficits in balance and motor coordination and altered social behaviors in offspring. In the present study, we have investigated the effect of maternal diabetes and insulin treatment on the cerebellar volume and morphogenesis of the cerebellar cortex of rat neonates during the first two postnatal weeks. Sprague Dawley female rats were maintained diabetic from a week before pregnancy through parturition.
View Article and Find Full Text PDFInsulin-like growth factor-1 (IGF-1) has an important role in development of the central nervous system (CNS). Maternal diabetes is associated with a higher risk of developmental abnormalities in their offspring including motor dysfunction and learning deficits. The present study aimed to investigate the effects of maternal diabetes on the distribution pattern of IGF-1 receptor (IGF-1R) in the developing rat cerebellar cortex.
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