glycogen has been researched along with Cognitive-Dysfunction* in 2 studies
2 other study(ies) available for glycogen and Cognitive-Dysfunction
| Article | Year |
|---|---|
Long-term light and moderate exercise intervention similarly prevent both hippocampal and glycemic dysfunction in presymptomatic type 2 diabetic rats.
A prediabetic population has an increased risk of cognitive decline and type 2 diabetes mellitus (T2DM). This study investigated whether the progression of memory dysfunction and dysregulated brain glycogen metabolism is prevented with 4 mo of exercise intervention from the presymptomatic stage in a T2DM rat model. Memory function and biochemical and molecular profiles were assessed in the presymptomatic stage of Otsuka-Long-Evans-Tokushima fatty (OLETF) rats, a T2DM model, with Long-Evans Tokushima (LETO) rats as genetic control. These rats were subjected to light- or moderate-intensity treadmill running for 4 mo with repetition of the same experiments. Significant hippocampal-dependent memory dysfunction was observed in the presymptomatic stage of OLETF rats, accompanied by downregulated levels of hippocampal monocarboxylate transporter 2 (MCT2), a neuronal lactate-transporter, without alteration in hippocampal glycogen levels. Four months of light or moderate exercise from the presymptomatic stage of T2DM normalized glycemic parameters and hippocampal molecular normalization through MCT2, glycogen, and brain-derived neurotrophic factor (BDNF) levels with the improvement of memory dysfunction in OLETF rats. A 4-mo exercise regimen from the presymptomatic stage of T2DM at a light and moderate intensities contributed to the prevention of the development of T2DM and the progression of cognitive decline with hippocampal lactate-transport and BDNF improvement. Topics: Animals; Blood Glucose; Brain-Derived Neurotrophic Factor; Cognitive Dysfunction; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Glycogen; Hippocampus; Humans; Lactates; Physical Conditioning, Animal; Prediabetic State; Rats; Rats, Inbred OLETF; Rats, Long-Evans | 2022 |
Restoring metabolism of myeloid cells reverses cognitive decline in ageing.
Ageing is characterized by the development of persistent pro-inflammatory responses that contribute to atherosclerosis, metabolic syndrome, cancer and frailty Topics: Adult; Aged; Aging; Animals; Cell Respiration; Cells, Cultured; Cognitive Dysfunction; Dinoprostone; Energy Metabolism; Glucose; Glycogen; Humans; Inflammation; Macrophages; Memory Disorders; Mice; Microglia; Mitochondria; Myeloid Cells; Receptors, Prostaglandin E, EP2 Subtype; Signal Transduction; Spatial Memory | 2021 |