ENVIRONMENTAL NANOPLASTIC ACCUMULATION AND NEURODEGENERATIVE DISEASE IN ANIMAL MODELS

Beatrice ZARRILLI^1,2, Nicola B. MERCURI^2,3, Rosaria MECCARIELLO¹, Ezia GUATTEO^1,2 | ¹University of Naples ‘Parthenope’, Department of Medical, Human Movement and Well-being Sciences, Naples, Italy; ²Experimental Neurology Laboratory, Fondazione Santa Lucia IRCCS, Rome, Italy; ³University of Rome Tor Vergata, Department of Systems Medicine, Rome, Italy

It is well known that production of plastic and deposition of waste worldwide are constantly increasing and microplastic contaminants in water and food supplies have been reported. Microplastics are commonly defined as particles with a diameter smaller than 5 mm but also include smaller nanoplastics particles of less than 1 μm size. Disposable polystyrene products, including packing materials, cups and cutlery, are the main objects accumulating in the environment that contribute to plastic pollution. As a consequence, small plastic particles are found in marine environments and presumably they derive from ultraviolet radiation exposures and plastic erosion. Experimental studies report that polystyrene nanoplastics can enter organisms inducing modification of tissue structure and function, such as endothelial leakiness and potentially compromise the blood-brain barrier in mammals.¹ Parkinson’s disease (PD) is a neurodegenerative disease characterized by progressive degeneration of a rather selective neuronal population located in the ventral midbrain that provides dopaminergic innervation within basal ganglia circuitry that controls voluntary movement. In PD, progressive loss of dopaminergic neurons (DAn) causes low dopamine (DA) levels in the brain and the appearance of resting tremor, bradykinesia and rigidity, cardinal motor symptoms of PD. Abnormal accumulation α-synuclein (α-syn) in Lewy bodies and Lewy neurites is an important characteristic of the neurodegenerative processes of substantia nigra pars compacta (SNpc) DAn neurons in Parkinson's disease (PD) and other synucleinopathies.^2,3 Animal models of PD display such accumulation of α-syn in the mesencephalic area, striatum and frontal cortex, accompanied to severe dysfunctions in the dorsolateral striatum. α-syn is a low-molecular weight protein, but in PD-affected tissues, it forms fibril structures that interact with damaged lipids deriving from various organelles, such as lysosomes and mitochondria.⁴ We will discuss recent literature on the role that specific types of nanoparticles, that are increasing in the environment, have in promoting α-syn aggregation and fibril elongation in neurons. We will also discuss the importance of model systems related to α-syn pathobiology to further explore different types of nanoparticles as potential toxins in PD.

References

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