Neuroborreliosis is a disorder of the central nervous system. It is a neurological manifestation of Lyme disease caused by a systemic infection of spirochetes of the genus Borrelia. The brain, spinal cord and other nerve pathways can and most often are invaded by the infection.

One part of the nervous system the bacterium love to inhabit is the brain. To do this they must get past the blood-brain barrier. (BBB)

The BBB has cells that let things in (things the brain requires) and lets out things such as waste products. The Borrelia has ways of getting through the BBB such as inside a product the brain requires (Trojan horse), by changing the proteins it is coated with so it is seen as a safe object to let through or damaging the junctions of the endothelial cells causing damage to the BBB in the process.

Quinolinic Acid (QUIN). Within the brain, QUIN is produced and released by infiltrating macrophages and activated microglia, the very cells that are prominent during neuroinflammation. It causes overstimulation of neurons, excitotoxic lesions, degradation of brain tissue and high levels of reactive oxygen in the brain.

The precursor to Quin, 3-HK, is also highly destructive because it generates free radicals.

QUIN’s impact on the brain is severe. Neurotransmitter interference, brain atrophy, damage to synaptic connections and even nerve death.

“Areas of the brain most sensitive to QUIN neurotoxicity are the hippocampus and striatum. Within these brain areas, some neuronal cell types are more sensitive than others, with cholinergic neuronal death in the striatum observed following QUIN injection.”Rafael Lugo-Huitrón et al (2013)

Why is this important?

It answers why Lyme sufferers suffer from memory and recall issues and confusion (Lyme Brain Fog). QUIN is often more of an issue for older members of our community as they often already have memory problems.

Another neuroborreliosis problem is indoleamine 2,3 dioxygenase or IDO for short.

IDO stimulation can significantly inhibit serotonin and melatonin levels. Melatonin is a powerful antioxidant and aid to sleep. Neuroborreliosis sufferers can find themselves with very low levels of melatonin. Low levels of serotonin can lead to becoming negative, obsessive, worried, irritable, sleepless, or depressed.

High levels of IDO can also lower Tryptophan which is an essential amino acid the body cannot synthesize. Studies have shown that Tryptophan can restore t cells ability to respond to bacterial infection, protect brain tissue, help with sleep and wellbeing. Supplementation is often needed.

Cytokine cascades can also be an issue with neuroborreliosis. Cytokines serve as molecular messengers between cells. Cytokines come in different forms and immunoregulatory and proinflammatory cytokines are the ones we are interested in.

“IL-1 beta is a key mediator of the inflammatory response. Essential for the host-response and resistance to pathogens, it also exacerbates damage during chronic disease and acute tissue injury. Lopez-Castejon, G., & Brough, D. (2011)

IL-1beta is stimulated by borrelial bacteria. Within the body, it is a common source of chronic and acute inflammation. This cytokine is closely involved in the increased sensitivity to pain.

“Overproduction of IL-1β is implicated in the pathophysiological changes that occur during different disease states, such as rheumatoid arthritis, neuropathic pain, inflammatory bowel disease, osteoarthritis, vascular disease, multiple sclerosis, and Alzheimer’s disease.” Braddock M, Quinn A. (2004)

Chronic pain is something that many Lyme sufferers face and reducing the cytokine IL-1beta cascade is important to the quality of life. There are effective herbs for attaining this result.

IL-6 is another cytokine causing inflammation. It easily crosses the blood-brain barrier and stimulates the production of PGE2 in the hypothalamus. This alters the body’s temperature regulation leading to temperature changes such as sudden excessive body heat. Many Lyme sufferers experience sweating at night leading to disturbed sleep.

This cytokine damages hippocampal tissue. It is especially damaging to endothelial cell junctions in the vascular system of the brain. Reducing IL-6 will reduce many of the neurological symptoms associated with Lyme and Lyme-like disease.

Other cytokines such as TNF-alpha are also involved in neuroborreliosis.

 

References

Braddock M, Quinn A. Targeting IL-1 in inflammatory disease: new opportunities for therapeutic intervention. Nat. Rev. Drug Discov. 2004;3:1–10

Lopez-Castejon, G., & Brough, D. (2011). Understanding the mechanism of IL-1β secretion. Cytokine & growth factor reviews, 22(4), 189–195. doi:10.1016/j.cytogfr.2011.10.001

Rafael Lugo-Huitrón, Perla Ugalde Muñiz, Benjamin Pineda, José Pedraza-Chaverrí, Camilo Ríos, and Verónica Pérez-de la Cruz, “Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets,” Oxidative Medicine and Cellular Longevity, vol. 2013, Article ID 104024, 14 pages, 2013.