Abstract
While growing evidence suggests that the pathogenesis of Parkinson’s disease is heavily associated with the accumulation [1, 2] and transmission [3, 4] of α-synuclein (α-syn) aggregates in the midbrain, no anti-fibrillation agents have been developed to treat the disease for the clinical practice. In this chapter, we highlight that graphene quantum dots (GQDs) prevent fibrillation of α-syn and directly interact with mature fibrils, inducing their dissociation into monomers. In addition, GQDs can inhibit the loss of neurons and synaptic proteins, reduce the formation of Lewy body and Lewy neurite, alleviate mitochondrial dysfunctions and sequential subcellular damages, and block neuron-to-neuron transmission of α-synucleinopathy induced by preformed α-syn fibrils [5, 6]. We also fount out, in vivo, that GQDs pass through the blood–brain barrier (BBB) and protect against the loss of dopamine producing neurons provoked by exogenous α-syn preformed fibrils, innate α-syn fibrillation by transgenic deficits, Lewy body/Lewy neurite formation and behavioral dysfunctions.
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