Ketone bodies (specifically β-Hydroxybutyrate) have been the recent topic of research for their possible therapeutic neurotropic effects in various neurodegenerative diseases, such as Parkinson’s disease, dementia, and seizures.  With glucose deprivation, as seen with fasting/prolonged exercise, these lipid-derived molecules deliver energy to neurons and other cells.  To determine if β-Hydroxybutyrate is a therapeutic option, additional in-silico, in vitro and in vivo research on ketone bodies is currently required.   In the current study, hippocampal HT-22 cells were treated with β-hydroxybutyric acid at different doses to elucidate the neurotropic effects.  Markers of oxidative stress, mitochondrial function and apoptosis were investigated. Using computational pharmacokinetic and molecular modeling software, we validated the pharmacokinetic effects and pharmacodynamic (NMDA and acetylcholinesterase) interactions of β-hydroxybutyric acid. Using a moderate dose, the ketone body (β-hydroxybutyric acid) showed significant dose-dependent increase in HT-22 cells.  β-hydroxybutyric acid exhibited an antioxidant effect by decreasing prooxidant stress (i.e. reactive oxygen species, nitrite content) and increasing glutathione content, leading to decreased lipid peroxidation. Moreover, β-hydroxybutyric acid improved mitochondrial functions by increasing Complex-I and Complex-IV activities. Additionally, β-hydroxybutyric acid significantly decreased apoptosis, as seen by reduction in caspase-1 and caspase-3 activities. The computational studies demonstrate that β-hydroxybutyric acid can interact with NMDA receptors and cholinesterase enzyme, the prime pharmacodynamic targets for cognitive impairment.  This further validates its oral absorption and distribution into the central nervous system, thereby validating its use in humans. Thus, this study highlights the neuroprotective effects of ketone bodies in cognitive-related neurodegenerative diseases.