Like the waistband of your pants after Thanksgiving dinner, neurons have to be able to stretch and then return to shape. On page 269 Hammarlund et al. pinpoint the protein that confers this springiness, showing that neurons lacking the molecule fracture.

Movements such as bending your elbow put strain on neurons, but the source of the cells' elasticity has been a mystery. Hammarlund et al. suspected that the protein β-spectrin was involved. In red blood cells, the protein weaves into a mesh that supports the cell membrane, enabling erythrocytes to rebound after being crushed and dented during their travels through the circulatory system.

The researchers tested spectrin's function in neurons by observing nematodes that lack the protein. In embryonic worms, neurons grew normally between the animals' two nerve cords, indicating that spectrin isn't necessary for development. But after the worms hatched, their neurons began to display defects such as abnormal branching, frequent breaks, and signs of new growth, which doesn't normally occur after the embryonic stage. By tracking individual neurons, the scientists demonstrated that the breaks came first; the aberrant growth and misguided branches followed as worms attempted to repair the severed cells.

To determine whether movement snaps the neurons, the researchers scrutinized paralyzed animals. Few of their neurons broke. Hammarlund et al. conclude that the fragility of spectrin-lacking neurons might explain some kinds of neurodegenerative diseases. For example, patients with spinocerebellar ataxia type 5—an inherited form of paralysis that ran in Abraham Lincoln's family—carry a faulty β-spectrin gene. Neurons might deteriorate in these patients because they break first, the researchers suggest.