This shows a brain.
Study results revealed a significant reduction in both inflammatory markers and of cell death. Credit: Neuroscience News

Treatment Relieves Chronic Lyme Disease’s Neurological Symptoms

Summary: Fibroblast growth factor receptor inhibitors, commonly used in cancer treatment, could effectively reduce neurological symptoms in patients with post-treatment Lyme disease syndrome. The study shows these inhibitors can decrease inflammation and cell death in brain and nerve tissues affected by Lyme disease.

This discovery paves the way for potential treatments aimed at the persistent neuroinflammation seen in some patients after standard antibiotic therapy. With promising initial results, further research is essential to move these findings from the lab to clinical applications.

Key Facts:

  1. Lyme disease can cause persistent neurological symptoms such as memory loss and fatigue, known as post-treatment Lyme disease syndrome, even after antibiotics.
  2. The study found that targeting FGFR pathways with specific inhibitors can significantly reduce inflammation and neuronal damage in tissue samples infected with Lyme disease bacteria.
  3. The research, supported by the Bay Area Lyme Foundation and resources from the Tulane National Primate Research Center, marks a critical step toward developing new interventions for chronic Lyme disease complications.

Source: Tulane University

Tulane University researchers have identified a promising new approach to treating persistent neurological symptoms associated with Lyme disease, offering hope to patients who suffer from long-term effects of the bacterial infection, even after antibiotic treatment.

Their results were published in Frontiers in Immunology

Lyme disease, caused by the bacterium Borrelia burgdorferi and transmitted through tick bites, can lead to a range of symptoms, including those affecting the central and peripheral nervous systems.

While antibiotics can effectively clear the infection in most cases, a subset of patients continues to experience symptoms such as memory loss, fatigue, and pain—a condition often referred to as post-treatment Lyme disease syndrome. 

Principal investigator Geetha Parthasarathy, PhD, an assistant professor of microbiology and immunology at the Tulane National Primate Research Center, has discovered that fibroblast growth factor receptor inhibitors, a type of drug previously studied in the context of cancer, can significantly reduce inflammation and cell death in brain and nerve tissue samples infected with Borrelia burgdorferi.

This discovery suggests that targeting FGFR pathways may offer an exciting new therapeutic approach to addressing persistent neuroinflammation in patients with post-treatment Lyme disease syndrome.  

“Our findings open the door to new research approaches that can help us support patients suffering from the lasting effects of Lyme disease,” Parthasarathy said.

“By focusing on the underlying inflammation that contributes to these symptoms, we hope to develop treatments that can improve the quality of life for those affected by this debilitating condition.”

Researchers treated nerve tissue with live or inactivated Borrelia burgdorferi, followed by an application of FGFR inhibitors. Study results revealed a significant reduction in both inflammatory markers and of cell death. 

While further research is needed to translate these findings into clinical treatments, the study represents an important step forward in understanding and potentially managing the complex aftermath of Lyme disease.

Funding: This study was funded by the Bay Area Lyme Foundation and supported with resources from the Tulane National Primate Research Center base grant of the National Institutes of Health, P51 OD011104. 

About this Lyme disease and neuropharmacology research news

Author: Keith Brannon
Source: Tulane University
Contact: Keith Brannon – Tulane University
Image: The image is credited to Neuroscience News

Original Research: Open access.
Fibroblast growth factor receptor inhibitors mitigate the neuropathogenicity of Borrelia burgdorferi or its remnants ex vivo” by Geetha Parthasarathy et al. Frontiers in Immunology


Fibroblast growth factor receptor inhibitors mitigate the neuropathogenicity of Borrelia burgdorferi or its remnants ex vivo

In previous studies, we showed that fibroblast growth factor receptors (FGFRs) contribute to inflammatory mediator output from primary rhesus microglia in response to live Borrelia burgdorferi.

We also demonstrated that non-viable B. burgdorferi can be as pathogenic as live bacteria, if not more so, in both CNS and PNS tissues. In this study we assessed the effect of live and non-viable B. burgdorferi in inducing FGFR expression from rhesus frontal cortex (FC) and dorsal root ganglion (DRG) tissue explants as well as their neuronal/astrocyte localization.

Specific FGFR inhibitors were also tested for their ability to attenuate inflammatory output and apoptosis in response to either live or non-viable organisms. Results show that in the FC, FGFR2 was the most abundantly expressed receptor followed by FGFR3 and FGFR1.

Non-viable B. burgdorferi significantly upregulated FGFR3 more often than live bacteria, while the latter had a similar effect on FGFR1, although both treatments did affect the expressions of both receptors.

FGFR2 was the least modulated in the FC tissues by the two treatments. FGFR1 expression was more prevalent in astrocytes while FGFR2 and FGFR3 showed higher expression in neurons.

In the DRG, all three receptor expressions were also seen, but could not be distinguished from medium controls by immunofluorescence. Inhibition of FGFR1 by PD166866 downregulated both inflammation and apoptosis in both FC and DRG in response to either treatment in all the tissues tested.

Inhibition of FGFR1-3 by AZD4547 similarly downregulated both inflammation and apoptosis in both FC and DRG in response to live bacteria, while with sonicated remnants, this effect was seen in one of the two FC tissues and 2 of 3 DRG tissues tested.

CCL2 and IL-6 were the most downregulated mediators in the FC, while in the DRG it was CXCL8 and IL-6 in response to FGFR inhibition. Downregulation of at least two of these three mediators was observed to downregulate apoptosis levels in general.

We show here that FGFR inhibition can be an effective anti-inflammatory treatment in antibiotic refractive neurological Lyme. Alternatively, two biologics may be needed to effectively curb neuroinflammation and pathology in the CNS and PNS.

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