Exploration of brain energy demand and neuronal aging: implications for tauopathies, neuroprotection

The link between brain energy consumption and neuronal aging has been explored at the cellular and molecular levels. The brain is described as a “selfish organ”, as previously indicated in recent publications, demanding energy from peripheral organs to avoid a reduction of its energy expenditure. Aging is the main risk factor for neurodegenerative disorders, like tauopathies, related to neuronal energy changes. Thus, preventing, delaying, or reversing those changes should be a suitable way to carry out neuroprotection. Finally, possible therapies using as targets neuronal proteins like folate receptor alpha, GDF15 receptor, or tau protein, which are related to mitochondrial function and dysfunction, are proposed.