Table 1.

Examples of neurotoxic effects and mechanisms caused by environmental NPs

Nanoparticle	Mechanism and relevance to neurodegeneration
Iron oxides: magnetite (Fe3O4) iron oxide (Fe2O3),	Axonal transport and bypass the BBB via the nasal olfactory epithelium [222, 255, 256]
	Daily exposure affects synaptic transmission and nerve conduction, causing neural inflammation, apoptosis, induced neural antioxidant responses, and immune cell infiltration [257]
	Disrupted Fe homeostasis [258, 259], release of free Fe ions to catalyze the production of reactive oxygen species (ROS) through the Fenton reaction [249, 260] as well as the promotion of amyloid-β toxicity, as shown in vitro [261]
Silicon dioxide (SiO2)	Increased oxidative stress and altered microglial function; deleterious effects on the striatum and dopaminergic neurons [262]
	Intranasal administration in a mouse model lead to cognitive dysfunction and impairment, synaptic changes as well as pathologies similar to neurodegeneration [263]
	Induction of neuron depolarization in a cell culture model; no detected change in gene expression [264]
	PD-like behavioral changes in SiO2 NP-exposed Zebrafish model [265]
	Dose-dependent cytotoxicity and AD-like pathology in vitro [266]
Titanium oxide (TiO2)	Absorption and translocation into the brain by any portal of entry. Can further cross the placental barrier and accumulate in the fetal brain, causing impairments in the fetal brain development [267]
	Damage to BBB and induction of inflammatory response [268, 269]
	Exposure precipitates the development of neuropathological findings of early PD, AD and ALS, some of which appear to be manifested symptomatically [221, 253, 270, 271]
Nickel (Ni)	Ni NPs increased (Aβ)40 and Aβ42 levels in murine brains [272]