Gigp-40.mp4 Link

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This paper explores the role of glycogen as a metabolic fuel source within neurons, specifically focusing on Glycogen-Dependent Glycolytic Plasticity (GDGP). Recent studies using sensors like HYlight in models such as Caenorhabditis elegans have identified that neurons can utilize glycogen to regulate glycolytic states during periods of high activity or transient hypoxia. This study highlights the essential role of PYGL-1, an ortholog of human glycogen phosphorylase, in sustaining this plasticity. Introduction

Glycogen serves as a direct fuel source to sustain glycolytic plasticity and synaptic function in vivo. The inability to utilize GDGP is associated with deficiencies in synaptic vesicle recycling during hypoxia. GIGP-40.mp4

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Traditionally, neurons were thought to rely primarily on blood-glucose-derived glucose, with astrocytes managing glycogen storage. However, evidence now indicates that neurons can engage in their own glycogen-dependent glycolytic plasticity (GDGP) to meet sudden metabolic demands. This paper investigates how GDGP operates, specifically in mitigating the effects of mitochondrial dysfunction. Findings on GDGP Mechanisms

Neurons regulate glycolysis dynamically in response to metabolic stress. This study highlights the essential role of PYGL-1,

Glycogen-Dependent Glycolytic Plasticity in Neuronal Function (GDGP)