Lyme Disease Pathology – Central Nervous System

lyme cns neuroborreliosis brainThe spread of the Lyme disease bacteria into the central nervous system varies in incidence and speed between individuals but when it does happen the spirochaetes may fundamentally alter brain function. It appears that astrocytes in the brain are involved in the pathogenesis of Lyme disease as these are glial cells providing support for endothelial cells that constitute the blood-brain barrier that protects the brain from damage by closely guarding entrance to brain circulation. The astrocytes are also important in maintaining nutrient supply to brain tissue, and in the repair process, and scarring, following trauma to the spinal cord or brain itself. The Borrelia bacteria induce astrogliosis in the astrocytes, a process where the cells rapidly reproduce and then die (proliferation followed by apoptosis). The effectiveness of the blood-brain barrier, the supply of nutrients to neural tissue, and the balance of ions in the brain can all be compromised through such events.


Neurotoxins and Lyme Disease

The secretory activities of brain cells are also adversely affected which is thought to contribute to some of the psychological and cognitive manifestations of Lyme disease. The spirochaetes can induce astrocytes and microglia to produce toxic substances such as quinolinic acid and specific cytokines interleukin-6 and Tumor necrosis factor-alpha, which damage nerve cells and can lead to the symptoms of fatigue and malaise in Lyme disease patients along with cognitive deficits such as memory impairment and poor concentration. Alterations in neurotransmitter function are also implicated in the development of some Lyme disease symptoms such as stress, anxiety, and sleep disturbance. There is some evidence showing that Borrelia bacteria induce the chronic elevated secretion of stress hormones such as cortisol which then reduce the effects of neurotransmitters and cause neurohormone disruption.

Antidepressants and Lyme Disease Pathology

Glucocorticoids and catecholamines are those neurohormones thought to be involved in this process and, with stem cell research recently revealing the benefits of anti-depressants such as sertraline (Zoloft) to be due to their effects on glucocorticoids, it appears likely that dysregulation of these pathways is a key factor in some symptoms of Lyme disease. Reduced levels of tryptophan, a serotonin-precursor, have also been observed in those with infectious diseases affecting the central nervous system, such as Lyme disease. Low levels of serotonin in the brain are connected to symptoms similar to those found in neuropsychiatric disorders that arise in patients with Lyme Borreliosis.

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