This research aims to tackle the question of how damaged neurons exert their own protection and regeneration. This question might be viewed as a mirror opposite question to how damaged neurons die, an unsolved mystery. However, we think that common or similar molecular mechanisms can be utilized to answer these two questions. Therefore, we think that answering our primary question can also contribute to understanding how neurons die.
Neuron, a cell type that consists of the neural system, contains three major structural compartments; a long single protrusion from the cell body called "axon," multiple protrusions from the cell body with relatively short length than axon called "dendrites," and cell body. Axons release various molecules, including amino acids, and dendrites receive those to achieve transmission of information among neurons. This event enables animals to recognize, memorize, and act appropriately. Currently, there are no treatment for complete cure of neuronal disease, including Alzheimer's and Parkinson's disease, and neuronal injury, including brain trauma and spinal cord injury. One of the common phenomena seen in the level of neurons is that they become structurally "bizarre" and "weak." In other words, neurons become unable to (1) properly release molecules for information transmission, (2) properly receive those molecules, or (3) are completely eliminated from the neural system. This research aims to clarify how these features described in (1)-(3) emerge at the molecular level by focusing on the structural changes of "weakening" neurons. In addition, we aim to clarify concepts for drug development that can repair (regenerate) "weakened" neurons observed in neuronal diseases and injury in the future.