Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease, with an incidence of 8-18 cases per 100,000 per year and currently about 125,000 cases in the UK. While lifestyle and genetic risk factors for Parkinson’s disease have been identified, the aetiology remains unclear. The current treatment options are limited to the management of symptoms. Iron is misdistributed and accumulates in the affected brain regions (particularly the substantia nigra) as the disease progresses. Iron chelation has been identified as a treatment that slows down disease progression, demonstrating promising results in two clinical trials. Currently available iron chelators only enter the brain to a very limited extent, which restricts their use for the treatment of Parkinson’s disease due to low effective doses achieved in the brain and potential systemic side effects. This thesis focused on the development of novel iron chelators that have been conjugated to sugars. In principle, this strategy could lead to the targeting of molecules to the brain and increase their penetration by facilitated transport across the blood-brain barrier by the glucose transporter GLUT1. The molecules are based on the 3-hydroxypyridin-4-one scaffold, which is the basis of the clinically used iron chelator deferiprone. Hydroxypyridinone iron chelators could be linked to the sugars via ether, amide and triazole linkers, but the deprotection of the resulting conjugates could only be achieved for some molecules, while others could not be successfully deprotected without degradation of the desired conjugate. Thirteen molecules were tested in blood-brain barrier assays based on primary cells from porcine brain endothelial microvessels. The tested chelators did not, however show greater blood-brain barrier permeability when compared to similar non-glycosylated chelators. Instead, permeability was low and correlated with the substances’ lipophilicity. This indicates that glycosylation alone is not sufficient for the transport of the conjugates and may hinder permeability. In order to increase a compound’s brain permeability by glucosylation, the transporter’s substrate binding specificity needs to be considered.