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d galactose/atrofia
O link é salvo na área de transferência
Página 1 a partir de 79 resultados
D-galactose-induced aging does not cause further deterioration in brain pathologies and cognitive decline in the obese condition
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Largely as a consequence of changes in modern lifestyle, a significant proportion of global population have become obese. When obese people grow old, pathologies aggravate neurodegeneration. Several studies have demonstrated that both aging and obesity have deleterious impact on brain. However, the
Impairments of tight junctions are involved in D-galactose-induced brain aging.
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Impairments of tight junctions are implicated in the course of various age-related neurodegenerative disorders. Chronic injection of D-galactose can cause a progressive deterioration in learning and memory capacity and serve as an animal model of aging. To investigate the involvement of tight
Chronic systemic injection of D-galactose impairs the septohippocampal cholinergic system in rats.
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Accumulated evidence indicates chronic systemic injection of D-galactose mimics aging progress induced by oxidative stress. We addressed whether memory impairment in this model was associated with the cholinergic septohippocampal degeneration. Rats injected with D-galactose for 6 weeks showed
Galactose and its Metabolites Deteriorate Metaphase II Mouse Oocyte Quality and Subsequent Embryo Development by Disrupting the Spindle Structure.
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Premature ovarian insufficiency (POI) is a frequent long-term complication of classic galactosemia. The majority of women with this disorder develop POI, however rare spontaneous pregnancies have been reported. Here, we evaluate the effect of D-galactose and its metabolites, galactitol and galactose
Preventive effects of taurine against d-galactose-induced cognitive dysfunction and brain damage.
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Oxidative stress arising from life processes or environmental influences and its resultant cellular dysfunctions are major causes of neurodegenerative disorders. The objectives of this study were to investigate whether taurine (Tau) can prevent d-galactose-induced cognitive dysfunction and brain
The Effects of Light and Moderate Intensity Exercise on the Femoral Bone and Cerebellum of d-Galactose-Exposed Rats.
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Aging causes the degeneration of organs of the locomotor system, including the cerebellum and bones. Exercise may reverse this deterioration. d-galactose has been frequently used in rodents to accelerate aging. The present study aimed at investigating the effects of exercise on cerebellar and serum
Kinetin inhibits apoptosis of aging spleen cells induced by D-galactose in rats.
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Kinetin (Kn) is a cytokinin growth factor that exerts several anti-aging and antioxidant effects on cells and organs. To investigate the mechanism underlying apoptotic events in aging cells induced by D-galactose (D-gal), we examined the effect of Kn delivered via nuchal subcutaneous injection on
Defective Central Immune Tolerance Induced by High-Dose D-Galactose Resembles Aging.
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D-Galactose (D-Gal) promotes accumulation of reactive oxygen species and formation of advanced glycation end-products, ultimately resulting in oxidative stress. D-Gal has been widely used to induce accelerated aging in anti-aging medical research. Although thymic epithelial cells are particularly
Activation of Wnt/β-catenin signaling by lithium chloride attenuates d-galactose-induced neurodegeneration in the auditory cortex of a rat model of aging.
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Degeneration of the central auditory system, which is characterized by reduced understanding of speech and source localization of sounds, is an important cause of age-related hearing loss (presbycusis). Accumulating evidence has demonstrated that Wnt/β-catenin signaling plays an essential role in
Resveratrol ameliorates thymus senescence changes in D-galactose induced mice
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Thymic microenvironment plays an important role in the development of T cells. The decrease of thymic epithelial cells is the main cause of age-related thymic atrophy or degeneration. Resveratrol (RSV), a phytoalexin produced from plants, has been shown to inhibit the adverse effects of dietary
Tuna Oil Alleviates d-Galactose Induced Aging in Mice Accompanied by Modulating Gut Microbiota and Brain Protein Expression.
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To discern whether tuna oil modulates the expression of brain proteins and the gut microbiota structure during aging induced by d-galactose, we generated an aging mouse model with d-galactose treatment, and the mice showed aging and memory deterioration symptoms according to physiological and
Selective pericyte degeneration in the retinal capillaries of galactose-fed dogs results from apoptosis linked to aldose reductase-catalyzed galactitol accumulation.
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Galactose-fed dogs develop retinal capillary changes similar to diabetic retinopathy with pericyte degeneration as the initial lesion. This is followed by the formation of microaneurysms, hemorrhages, and some areas of acellularity. To investigate the mechanisms for selective pericyte degeneration,
Pathological and biochemical alterations of astrocytes in ovariectomized rats injected with D-galactose: a potential contribution to Alzheimer's disease processes.
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Astrocytes are implicated in the pathological changes of Alzheimer's disease. Our previous studies have demonstrated that estrogen deprivation and oxidative stress act synergistically to accelerate the progress of Alzheimer's disease. Long-term D-galactose injection combined with ovariectomy may
Hippocampal neurochemical changes in senescent mice induced with chronic injection of D-galactose and NaNO₂: an in vitro high-resolution NMR spectroscopy study at 9.4T.
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Proton magnetic resonance spectroscopy (¹H-MRS) has been used to provide useful information about the neurochemical changes reflecting early pathological alterations in Alzheimer's disease (AD) brain. In this study, we have longitudinally measured the hippocampal neurochemical profile in vitro in
Consequences of recurrent phosphate trapping induced by repeated injections of 2-deoxy-D-galactose. Biochemical and morphological studies in rats.
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2-Deoxy-D-galactose, in a dose of 3 mmol/kg, was administered intraperitoneally twice daily to young rats for periods up to 12 weeks. This dosage schedule resulted in recurrent phosphate trapping predominantly in liver. UTP deficiency was excluded by simultaneous uridine injections. Phosphate
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