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Neuronal energy metabolism refers to the complex set of biochemical processes by which neurons generate, utilize, and regulate their supply of metabolic resources—primarily ATP—to support high-demand functions such as synaptic activity, maintenance of membrane potentials after depolarization, neurotransmitter cycling, vesicle recycling, axoplasmic transport, and redox balance. The brain is highly metabolically active; although it constitutes only a small fraction of body mass (~2%), it accounts for over 20% of total oxygen consumption. Neurons themselves are responsible for 75–80% of this energy use. Energy is primarily derived from glucose oxidation via glycolysis and mitochondrial respiration but can also involve lactate shuttling from astrocytes during periods of high activity. Disruptions in these metabolic pathways are implicated in neurodegenerative diseases like Parkinson’s disease and cognitive decline with aging. However, "neuronal energy metabolism" is not itself a discrete therapeutic target but rather an umbrella term describing essential cellular processes involving many molecular players including enzymes (e.g., hexokinase), organelles (mitochondria), transporters (glucose/lactate transporters), signaling molecules/regulators involved in neurovascular coupling and metabolic adaptation[1][2][4][5][6]. Because "neuronal energy metabolism" does not refer to one specific molecule or receptor but instead encompasses multiple pathways critical for neuron function—and because there is no canonical abbreviation nor direct drug targeting—it should not be considered a standard therapeutic target entry.
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