Through a complex molecular crosstalk, Ocimum sanctum Linn (tulsi) has shown notable neuroprotective effects in a variety of neurodegenerative disease models. The ability of tulsi extract to maintain dendritic branching in substantia nigra neurons—a region that is significantly impacted in models of Parkinson’s disease—indicates that it can prevent and mitigate behavioral abnormalities and neuronal damage brought on by stress. Tulsi extract may help with memory and cognitive processes because it stabilizes the expression of choline acetyltransferase (ChAT), a crucial enzyme in cholinergic neurotransmission, and increases the viability of neuronal cells exposed to neurotoxic agents in vitro. Tulsi’s strong anti-inflammatory and antioxidant qualities are responsible for its neuroprotective effects, as they aid in reducing inflammation and oxidative stress, two key factors in the pathophysiology of neurodegenerative diseases. Furthermore, tulsi has been demonstrated to modify the lipid profile of the brain after ischemic injury, changing important lipid species involved in neuronal repair and neurotransmission, thus promoting recovery from stroke-like damage. Tulsi and its bioactive compounds may reduce β-amyloid oligomerization and inhibit neuronal apoptosis by downregulating caspase-3 and -9 at the molecular level, providing protection against neurotoxicity similar to Alzheimer’s disease. All of these results point to tulsi’s neuroprotective potential, which is mediated by anti-inflammatory, antioxidant, lipidomic, and anti-apoptotic pathways. As such, it is positioned as a promising adjunctive therapy option for neurodegenerative diseases.