Thiamine and Parkinson's disease

Abstract Parkinson's disease (PD) is the second most common form of neurodegeneration in the elderly population. PD is clinically characterized by tremors, rigidity, slowness of movement and postural imbalance. A significant association has been demonstrated between PD and low levels of thiamine in the serum, which suggests that elevated thiamine levels might provide protection against PD. Genetic studies have helped identify a number of factors that link thiamine to PD pathology, including the DJ-1 gene, excitatory amino acid transporters (EAATs), the α-ketoglutarate dehydrogenase complex (KGDHC), coenzyme Q10 (CoQ10 or ubiquinone), lipoamide dehydrogenase (LAD), chromosome 7, transcription factor p53, the renin–angiotensin system (RAS), heme oxygenase-1 (HO-1), and poly(ADP-ribose) polymerase-1gene ( PARP-1 ). Thiamine has also been implicated in PD through its effects on L-type voltage-sensitive calcium channels (L-VSCC), matrix metalloproteinases (MMPs), prostaglandins (PGs), cyclooxygenase-2 (COX-2), reactive oxygen species (ROS), and nitric oxide synthase (NOS). Recent studies highlight a possible relationship between thiamine and PD. Genetic studies provide opportunities to determine which proteins may link thiamine to PD pathology. Thiamine can also act through a number of non-genomic mechanisms that include protein expression, oxidative stress, inflammation, and cellular metabolism. Further studies are needed to determine the benefits of using thiamine as a treatment for PD.