CARS imaging shows calcium ions may have role in multiple sclerosis
11 July 2007
Researchers at Purdue University have discovered that
calcium ions could play a crucial role in multiple sclerosis by activating
enzymes that degrade the fatty sheath that insulates nerve fibres.
researchers employed an imaging technique called coherent anti-Stokes Raman
scattering, or CARS, that uses interfering laser beams to vibrate and
identify selected molecules. In this study they showed how the myelin sheath
is degraded by a molecule called lysophosphatidylcholine (LPC).
findings suggest that LPC causes sheath degradation by allowing an influx of
calcium ions into the myelin. The increased concentration of calcium ions
then activates two enzymes — calpain and cytosolic phospholipase A2 — which
break down proteins and fatty molecules in the myelin called lipids.
Cytosolic phospholipase A2 cuts off one of the two tails of these lipid
molecules and turns them into LPC, amplifying the effect and further
degrading the myelin.
Learning exactly how the myelin sheath is degraded
might enable scientists to determine how to halt disease progress and
reverse damage by growing new myelin, said Ji-Xin Cheng, an assistant
professor in Purdue University's Weldon School of Biomedical Engineering and
Department of Chemistry.
LPC, does not cause multiple sclerosis, but it is
used extensively in laboratory research to study the deterioration of
myelin, which insulates nerve fibres and enables them to properly conduct
"Although multiple sclerosis has been studied for many years, nobody knows
exactly how the disease initially begins. The pathway is not clear. It is
possible that the same pathway causes myelin degradation in people suffering
from multiple sclerosis and spinal cord injuries," Cheng said.
research findings were published in the Journal of Neuroscience Research in
"The findings of this study will help us to identify key steps in the
progression of the demyelination, which is a hallmark of multiple
sclerosis," said Riyi Shi, a researcher at Purdue's Institute for Applied
Neurology and Center for Paralysis Research. "This information will also
facilitate the design of pharmaceutical interventions that slow down or even
reverse the development of the debilitating disease."