Certain chronic neurologic disorders, such as Parkinson’s disease, are caused by an insufficiency of the neurotransmitter dopamine secondary to the degeneration of substantia nigra dopaminergic neurons.¹ N-(α-Linolenoyl) tyrosine (NALT) is a simple α-amide conjugate between the ω-3 essential fatty acid α-linolenate and the amino acid tyrosine. α-Linolenate is an important precursor to docosahexaenoic acid (DHA), a prominent brain polyunsaturated fatty acid, while tyrosine is the metabolic precursor for neuronal dopamine synthesis. NALT was prepared as a method for enhancing central nervous system (CNS) dopamine content by facilitated transport of the tyrosine precursor across the blood-brain barrier.² In experimental rat models of dopamine insufficiency, NALT increased CNS dopamine levels and exhibited an activity profile consistent with an anti-Parkinson’s therapeutic agent.²

≥98%