axons

The fact that it is the most evolved neurons, the ones that have expanded dramatically in humans, suggest that what we’re seeing might be the ‘future.’ As neuronal diversity increases and the brain needs to process more and more complex information, neurons change the way they use myelin to achieve more.

Their recent findings shed new light on the mechanical properties of a critical brain protein and its role in the elasticity of axons, the long, tendril-like part of brain cells. This protein, known as tau, helps explain the apparent contradiction this elasticity presents. If axons are so stretchy, why do they break under the strain of a traumatic brain injury?

The implications for human health — although a long way down the road — are important, Rolls said. For example, in the case of stroke, when a region of the brain suffers blood loss, dendrites on brain cells are damaged and can be repaired only if blood loss is very brief. Otherwise, it is thought those brain cells die. But if those cells are able to regenerate dendrites, and if scientists learn how dendrite regrowth happens, researchers may be able to promote this process.

Mutations in the genes encoding the three proteins can lead to some neurological and mental disorders in humans. In many other diseases, the primary defect initiated by something else can alter the function of these three proteins – and particularly sodium channel transport and function – and ultimately disrupt the nerve impulse. If the sodium channel can’t conduct the nerve impulse anymore, that gives rise to symptoms of neurological disorders.

Using a form of magnetic resonance imaging, or MRI, researchers at the Indiana University School of Medicine and the Geisel School of Medicine at Dartmouth College found significant differences in brain white matter of varsity football and hockey players compared with a group of noncontact-sport athletes following one season of competition.

Researchers at Washington University School of Medicine in St. Louis have identified a chain reaction that triggers the regrowth of some damaged nerve cell branches, a discovery that one day may help improve treatments for nerve injuries that can cause loss of sensation or paralysis.

Brown University researchers have traced a genetic deficiency implicated in autism in humans to specific molecular and cellular consequences that cause clear deficits in mice in how well neurons can grow the intricate branches that allow them to connect to brain circuits.

Biologists at the University of California, San Diego have identified a new component of the cellular mechanism by which humans and animals automatically check the quality of their nerve cells to assure they’re working properly during development.

When the central nervous system is injured, oligodendrocyte precursor cells (OPC) migrate to the lesion and synthesize new myelin sheaths on demyelinated axons. Scientists at the Institute of Molecular Cell Biology at Johannes Gutenberg University Mainz (JGU) have now discovered that a distinct protein regulates the direction and movement of OPC toward the wound. The transmembrane protein NG2, which is expressed at the surface of OPCs and down-regulated as they mature to myelinating oligodendrocytes, plays an important role in the reaction of OPC to wounding.

“We don’t know precisely how information is encoded in the brain, but we presume that some signals are important and some are noise,” says senior author Vitaly Klyachko, PhD, assistant professor of cell biology and physiology. “Our theoretical model suggests that the changes we detected may make it much more difficult for brain cells to distinguish the important signals from the noise.”