A group of clever researchers from Cornell have studied the anti-neural antibody reactivity in the brain of patients who have “Post Lyme Disease Syndrome” as compared to healthy people who have recovered from Lyme disease (and a control group of healthy people who have not had Lyme disease) in an effort to analyze the immune system abnormalities with respect to lingering symptoms, and mechanical evidence of possible permanent damage to the brain and/or clues to treatment in the future.
“Post Lyme Disease Syndrome” is the politically correct diagnosis for a patient suffering with Lyme symptoms who has been treated in accordance with the “IDSA Guidelines.”
In truth, Chronic Lyme Disease and Post Lyme Disease Syndrome are indistinguishable from symptoms alone, in fact, I know many people who suffer from terrible rage over the light dose of antibiotics and short treatment as prescribed by IDSA that have left them completely disabled months or years later when it is possible they could have been completely cured with one or two more weeks of antibiotics according to some Lyme experts, or a stronger dosage.
As people are educating themselves, they will not stand by and watch their children forced out of school because of political posturing. They want answers and they want them now.
In some ways you can view Post Lyme Disease Syndrome as the IDSA foot soldier’s label for “I don’t know.” We would all prefer intellectual honesty, but that is just never going to happen.
However, a study such as this looking into the effects of the anti-neural antibody reactivity in those with PLDS gives us the good news that at least someone is asking the questions!
So the good news, (and the bad news) is that the study revealed abnormal behavior in the brain in both the healthy and unhealthy “previous” Lyme patients by assessing the extent of cross-reactivity of the anti-borrelia antibodies towards brain protein.
In other words, the Lyme spirochetes drill into the brain in such a way that is not easily destroyed by short courses of antibiotics – hence the “Post Lyme Disease Syndrome”. According to the study, “…the cross-reactivity was confirmed by immunohistochemical analysis, which showed anti-borrelia antibody binding to neurons and glial cells of the cerebral cortex, and the dorsal root ganglion.”
The researchers began with the following goals:
“The aim of this study was to begin a process of examining potential immune abnormalities in PLS that would be relevant to the reported neurologic and cognitive symptoms of affected patients.
“Results of the antibody analysis demonstrate the presence of a heightened, but apparently non-specific, production of antibodies to neural antigens in PLS. We speculate that these antibodies may either 1) be indicative of past injury to the nervous system during the active phase of the Lyme disease infection, resulting in the immune system being exposed to and activated by novel self antigens, or 2) point to the enhanced B cell mitogenic effect of the borrelia pathogen in cases of delayed treatment and prolonged infection in genetically predisposed individuals.
“As such, this study points to the presence of a differential immune response in PLS in comparison to healthy individuals.
“Obviously, these findings are preliminary and must be extended in future studies using a larger number of subjects and additional cohorts, including healthy individuals with past Lyme arthritis and neurologic Lyme, as well as patients with similar complaints and no history of Lyme disease.
“At this juncture, it is logical to assume that further study of immune system response in PLS is likely to yield more clues about the etiopathogenesis of the disease and provide insights that may pave the way for developing safe and effective treatments.”
As the research continued, there were surprises along the way that showed borrellia activity in the brain well after the treatment in both the healthy and unhealthy subjects.
Doesn’t that sound like chronic Lyme disease? If the infection is present, active and causing measurable reactions in the brain, are we imagining our symptoms?
The study continues:
“We can make some conjectures about the possible reasons for the observed increased antibody reactivity to self antigens in PLS.
“First, our experiments with affinity-purified antibodies generated in rabbits against B. burgdorferi antigens clearly show that anti-borrelia antibodies can cross-react with several neural proteins. A number of earlier studies have also demonstrated the potential for cross-reactivity of the anti-borrelia immune response towards neural antigens (Alaedini and Latov, 2005; Dai et al., 1993; Garcia-Monco et al., 1995; Maier et al., 2000; Sigal and Tatum, 1988).
“A portion of the observed anti-neural antibody reactivity in PLS patients is, therefore, likely to be the result of such cross-reactivity. However, the observed anti-neural antibody reactivity cannot be attributed solely to positive anti-borrelia serology, as increased anti-neural antibody reactivity was also seen in the borrelial seronegative PLS group.
“Second, considering the non-specific pattern of immunologic reactivity, the presence of these antibodies might signify an activated immunologic response to neural injury caused by the original borrelial infection or another disease. Tissue injury can, in fact, result in the release of auto-antigens and lead to an increase in post-translational modification of proteins and production of novel self-epitopes that elicit a strong immune response (Doyle and Mamula, 2005).
“Third, borrelial infection has been shown to be a potent polyclonal B cell activator, capable of inducing the non-specific proliferation and differentiation of antibody-secreting cells (Ma and Weis, 1993; Yang et al., 1992). The ability of borrelia to act as a B cell activator is likely to be enhanced the longer the infection is left untreated (Soulas et al., 2005).
“Therefore, the observed non-specific increase in autoreactive antibodies in PLS may be due to the mitogenic effect of the borrelial antigens, including OspA and OspB, and point to a possible association between post-Lyme disease symptoms and the duration of the course of active infection prior to treatment.
“Finally, immune abnormalities stemming from genetic predisposition might also play a significant role in the form of B cell and effector cell dysregulation that leads to elevated levels of released auto-antibodies (Hostmann et al., 2008).
“At this point, it is difficult to know what role, if any, the anti-neural antibodies might play in the pathogenesis of PLS. Several immune-mediated diseases of the nervous system, including multiple sclerosis, paraneoplastic nervous system disorders, autoimmune neuropathies, myasthenia gravis, and stiff-person syndrome, are associated with elevated levels of antibodies to neural antigens.
“A disease-causing role for such antibodies has been demonstrated in some of these disorders (Dalakas, 2008). In general, antibodies might have a pathogenic effect in the body through direct binding to a molecule and interference with its function, by activation of complement and initiation of an inflammatory response, or by inducing tissue injury through binding to Fc receptors on macrophages, neutrophils, and NK cells (Diamond et al., 2009).
“Considering the non-specific antibody response seen in the examined PLS cohort, however, a direct pathogenic role for the antibodies is doubtful. Nevertheless, even without a direct role, antibodies have the potential to be involved in disease mechanism through the activation of toll-like receptor pathways and secretion of various inflammatory molecules, which can affect the function of other cells responsible for neuro-psychiatric defects (Crow, 2007; Halperin, 2008; Nawa and Takei, 2006).
More sanctioned studies like this will spawn more…it is an event to be celebrated.