Alzheimer's disease (AD) damages both the way electrical charges travel within cells and the activity of neurotransmitters. In the brain of a AD patient, there are fewer nerve cells and synapses. Two main indicators of AD are neurofibrillary tangles and amyloid beta plaques in the brain. Amyloid beta attacks and kills the pathways in the neuron forest. Moreover, amyloid beta stimulates immune system and thus leads to inflammation and the collapse of the unhealthy cells.

Orderly parallel strands in the brain permit nutrients and essential proteins to move between cells. These strands are like railroad tracks. The protein tau is important to the normal function of the tracks.

In an AD brain, tau breaks down, collapses and forms tangles that prevent transmission along the tracks. The tracks fall apart and nutrients and essential proteins can not reach brain cells. As a result, the brain cells die.

According to a new study, researchers devised a new mitochondria-targeting ceria nanoparticle that can effectively inhibit the process of neuronal cell death.

It is known that mitochondria supplies energy for cells. Reactive oxygen species (ROS) are formed as a natural by-product of normal metabolism of oxygen. Abnormal production of ROS, resulting from mitochondrial dysfunction, can cause neuronal cell to die. Moreover, amyloid beta can lead to mitochondrial dysfunction and it's a possible reason of AD via abnormal production of ROS.

Ceria nanoparticles act as strong and recyclable ROS scavengers, eliminating abnormal ROS. The researchers synthesized a ceria nanoparticle, mitochondria-specific antioxidant, and examined its effect in suppressing the pathogenesis of AD in mice experiments. The study might lead to a potent therapeutic agent for AD.