How Lysophosphatidic Acid Could Help Monitor Multiple Sclerosis

Multiple sclerosis (MS), a chronic autoimmune disease of the central nervous system, continues to challenge researchers and clinicians due to its unpredictable course and elusive biomarkers. However, a 2018 study by Dongxiao Jiang and colleagues published in Neurological Research provides promising insights into a potential biomarker that could revolutionize MS monitoring and treatment evaluation: lysophosphatidic acid (LPA).

What Is Lysophosphatidic Acid (LPA)?
LPA is a lipid signaling molecule involved in many critical biological functions—such as cell survival, inflammation, and neural communication. It's not a newcomer to medical science; LPA has been implicated in diseases ranging from cancer to cardiovascular conditions. But only recently has it attracted attention in the context of neurological disorders like MS.

The Study: Measuring LPA in MS Patients
Jiang et al. conducted a clinical study involving 41 patients with relapsing-remitting MS (RRMS)—divided into those experiencing a relapse (21 patients) and those in remission (20 patients)—and a control group of 21 individuals with non-inflammatory neurological conditions like epilepsy and migraines.

The researchers measured LPA concentrations in both serum and cerebrospinal fluid (CSF) using a specialized phosphate assay before and after standard corticosteroid treatment in relapsing MS patients.

Key Findings
Elevated LPA During Relapse:
Patients experiencing a relapse had significantly higher LPA levels in both serum and CSF compared to patients in remission and control participants.

Serum LPA: 3.04 µmol/L in relapse vs. 2.31 µmol/L in remission

CSF LPA: 3.32 µmol/L in relapse vs. 2.43 µmol/L in remission

LPA Responds to Treatment:
Following corticosteroid therapy, LPA levels in relapsing patients decreased significantly, aligning more closely with levels seen during remission:

Serum LPA dropped from 3.04 to 2.19 µmol/L

CSF LPA dropped from 3.32 to 2.31 µmol/L

Biomarker Potential:

These changes suggest that LPA could serve as a biomarker not only for detecting MS relapse but also for monitoring treatment effectiveness.

Why LPA Matters in MS
The study links LPA to the inflammatory processes that drive MS progression. Inflammation in MS leads to the activation of immune cells, cytokine release, oxidative stress, and damage to the myelin sheath. LPA appears to amplify these effects by:

Activating microglia and macrophages
Stimulating phospholipase enzymes that increase inflammation

Contributing to demyelination and neural injury

Additionally, LPA is produced through enzymatic pathways that are upregulated during inflammation—such as those involving autotaxin, an enzyme previously found elevated in MS patients.

Limitations and Considerations
While the results are promising, the authors caution against over-reliance on LPA alone: The difference in LPA levels between relapse and remission was less than twofold, meaning LPA may not serve as a standalone diagnostic tool.

Sample size was modest (n=41 MS patients), and further validation in larger cohorts is needed.

Combining LPA with other biomarkers might yield a more accurate diagnostic panel.

Conclusion
This study sheds light on a potentially powerful biomarker for MS: lysophosphatidic acid. Its dynamic response to disease activity and treatment points toward new diagnostic and therapeutic pathways. While further research is essential, LPA could one day help clinicians predict relapses, monitor responses, and personalize treatments for individuals living with MS.

Disclaimer: This blog post is based on the provided research article and is intended for informational purposes only. It is not intended to provide medical advice. Please consult with a healthcare professional for any health concerns.

References:
Jiang D., Ju W., Wu X., & Zhan X. (2018). Elevated lysophosphatidic acid levels in the serum and cerebrospinal fluid in patients with multiple sclerosis: therapeutic response and clinical implication. Neurological Research. https://doi.org/10.1080/01616412.2018.1446256