Excessive lysophosphatidic acid can cause fetal hydrocephalus

Scientists in the United States recently reported that they used mice for experiments that found that fetal hydrocephalus may be caused by an excess of lysophosphatidic acid (LPA). This finding may help diagnose and treat fetal hydrocephalus.

Fetal hydrocephalus is a type of neural tube malformation caused by excessive accumulation of cerebrospinal fluid in the ventricular system, which can lead to neonatal brain damage, abnormal head size, and possible death. The current treatment is mainly through the surgical implantation of shunt devices to help discharge water, but the long-term effect is not ideal.

People have previously found that hydrocephalus is related to intracranial hemorrhage, but it is unclear how it works. Scientists at the Scripps Research Institute in the United States have discovered that lysophosphatidic acid, a normal component of blood, may be the key to the problem. Experiments have found that injecting lysophosphatidic acid into the mouse embryonic ventricle can cause symptoms similar to those of human fetal hydrocephalus. However, if a compound is injected in advance to prevent lysophosphatidic acid from binding to receptor molecules on the surface of brain cells, injection of lysophosphatidic acid will not cause hydrocephalus.

Lysophosphatidic acid is a normal component of serum and is secreted by platelets, fibroblasts, and adipocytes. It is a signal molecule with various biological functions and plays an important role in the development of neurons and other cells. If the lysophosphatidic acid is excessive, the activity of the brain cell surface receptor molecules will be abnormal, resulting in changes in the structure of the fetal brain during its formation.