Nanoparticle Neurotoxicity in Central Nervous System

The proliferation of engineered nanoparticles across medical, industrial and consumer applications has raised concerns over their potential impact on the central nervous system. Nanoparticles can translocate to the brain via inhalation, systemic circulation or direct olfactory pathways. Once in contact with neural tissues, they may disrupt the integrity of the blood–brain barrier, induce oxidative stress and provoke neuroinflammatory responses. At the cellular level, exposure can impair mitochondrial function, alter synaptic protein expression and trigger apoptotic pathways in neurons and glial cells. The global significance of these findings extends to occupational safety, environmental regulation and the design of safer nanomaterials. Understanding the balance between therapeutic benefits and unintended neurotoxic effects is crucial for the continued advancement of nanotechnology in health and industry.

Research from Nature Portfolio

In ageing rodent models exposed by inhalation to titanium dioxide nano-aerosol, investigators observed an age-dependent increase in blood–brain barrier permeability accompanied by elevated brain cytokine levels and reduced synaptophysin expression. Despite an absence of detectable nanoparticle deposition in the parenchyma, systemic inflammatory mediators were implicated in driving central effects. This work highlights how peripheral exposure to nanoparticles can elicit remote inflammatory signalling with functional consequences for neuronal activity and barrier physiology, particularly in vulnerable populations.

Nanoparticle Neurotoxicity in Central Nervous System publication trend

The graph below shows the total number of articles in nanoparticle neurotoxicity in central nervous system across all publications each year (not limited to Nature Index journals).

Technical terms

Blood–brain barrier: Cellular and molecular interface regulating passage between circulation and central nervous system.

Reactive oxygen species (ROS): Chemically reactive molecules derived from oxygen that can damage cellular components.

Oxidative stress: Imbalance favouring ROS over antioxidant defences, leading to cellular injury.

Neuroinflammation: Immune response within the central nervous system involving glial activation and cytokine release.

Tunnelling nanotubes: Filamentous structures enabling direct intercellular transfer of organelles and signals.

References

1. ROS/mtROS promotes TNTs formation via the PI3K/AKT/mTOR pathway to protect against mitochondrial damages in glial cells induced by engineered nanomaterials. Particle and Fibre Toxicology (2024).
2. Silica nanoparticles induce neurodegeneration-like changes in behavior, neuropathology, and affect synapse through MAPK activation. Particle and Fibre Toxicology (2018).
3. Brain Inflammation, Blood Brain Barrier dysfunction and Neuronal Synaptophysin Decrease after Inhalation Exposure to Titanium Dioxide Nano-aerosol in Aging Rats. Scientific Reports (2017).
4. Toxicity of metallic nanoparticles in the central nervous system. Nanotechnology Reviews (2019).
5. Neurotoxicity of Nanomaterials: An Up-to-Date Overview. Nanomaterials (2019).