This
article recently appeared in the December publication of Ticks and
Tick-borne Diseases, titled "Neuroborreliosis and acute encephalopathy:
The use of CXCL13 as a biomarker in CNS manifestations of Lyme
borreliosis"
Abstract:
We report the case of an 80-year-old patient with acute onset confusion initially suspected to reflect delirium in incipient Alzheimer's disease. Cerebrospinal fluid tests revealed an unusually severe form of neuroborreliosis, which resolved following antibiotic treatment. This was mirrored in the measurement of CXCL13, which is suggested as a complementary biomarker"
What is CXCL13 and how does it relate to other inflammatory molecules in the body that are produced during an infection? Here is an explanation from "How Can I Get Better?" Chapter 3, Lyme Disease Specifics and Treatment Options:
"Scientific research has shown that borrelia creates an inflammatory response in the body where molecules are produced, called inflammatory cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF- alpha), and interferon gamma. These can cause fatigue,
pain, headaches, memory and concentration problems, and mood swings. Specialized signaling proteins, called chemokines, such as CCL-2 and CXCL-13, are also produced during an infection. These proteins recruit specialized immune cells such as B cells to make antibodies at the site of the infection, including the central nervous system, during neuroinflammation. Cytokines and chemokines can both modulate immune
activation and inflammation as they direct immune cells to the sites of tissue injury and infection".
"The reason that alternative diagnostic techniques are necessary to diagnose neuroborreliosis is that MRI’s, SPECT scans and PET scans of the brain are not able to definitively determine if a patient has neurological Lyme disease. Physicians will therefore occasionally perform a spinal tap and look at markers in the spinal fluid to determine if Borrelia burgdorferi has invaded the CNS. Unfortunately, spinal taps also have their limitations. Although increased antibody production in the spinal fluid can be seen in early Lyme disease with a lymphocytic meningitis or encephalitis, in late stage neurological Lyme patients, patients can have normal cerebrospinal fluid (CSF) antibody studies. For example, Dr. Coyle and Dr. Schutzer studied 35 patients with specific Lyme Antigen (Osp A) in their cerebrospinal fluid, indicative of neurological Lyme disease. Of these patients studied, although the Lyme antigen was positive, 43% had no evidence of antibodies to Lyme in their CSF testing, and 47% had otherwise normal routine CSF analyses. 60% of these patients were also seronegative for Lyme disease when tested with standard blood tests, implying that a patient can have Lyme disease despite a negative blood test and a negative spinal tap. The authors concluded that, “neurologic infection by B. burgdorferi should not be excluded solely on the basis of normal routine CSF or negative CSF antibody analyses.”
• Coyle PK, Schutzer SE, Deng Z, Krupp LB, Belman AL, Benach JL, Luft BJ. Detection of Borrelia burgdorferi-specific antigen in antibody-negative cerebrospinal fluid in neurologic Lyme disease. Neurology. 1995 Nov;45(11):2010-5;
Patients may also be seronegative for Lyme disease because of sequestration of antibody in immune complexes.
• Schutzer SE, Coyle PK, Belman AL, Golightly MG, Drulle J. Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease. Lancet. 1990 Feb 10;335(8685):312-5;
In Chapter 13 of "How Can I Get Better? I discuss nine factors on the Horowitz Sixteen-Point MSIDS Map, which have all been published in the scientific literature in the past several years, that have been proven to be associated with Alzheimer’s disease, apart from genetic influences. These factors are affecting the neurocognitive functioning of large numbers of the general population. They include
1. Multiple infections (Borrelia burgdorferi, other spirochetes (B.
miyamotoi, denticola spirochetes in the mouth); similar spiral shaped organisms (Helicobacter pylori); Chlamydia pneumonia; Porphyromonas gingivalis; viruses (HSV-1, cytomegalovirus); and possibly fungal infections;
2. Immune Dysfunction/Autoimmunity: Brain-reactive autoantibodies
3. Inflammation: The Framingham Study found inflammation
and an increase in inflammatory cytokines to increase the risk of
Alzheimer’s disease.
4. Environmental Toxins and Neuroimmunotoxicology: In 2014,
JAMA Neurology reported that levels of the pesticide DDE were
3.8- fold higher in those with AD. Other environmental toxins like ozone and small- particulate matter have also been linked to Alzheimer’s dementia.
5. Diet: Lipid- based diets effectively combat Alzheimer’s disease in the mouse model, and increases in dietary intake of either flavonoids (blueberries) or the omega-3 FA (DHA) in fish enhances neurogenesis and memory.
6. Sleep disorders: Lack of sleep contributes to elevations in
inflammatory cytokines like IL-6, & microinfarcts in the brain
7. Hormonal Dysregulation: Numerous studies have documented
a strong association between diabetes and Alzheimer’s disease
and suggest that avoiding excess insulin may help prevent and
lessen the impact of the disease.
8. Rest and Restore: Meditation may reduce hippocampal- volume atrophy in mild cognitive impairment (MCI), while having a positive impact on brain regions most related to dementia.
9. Exercise: increases the size of the hippocampus and improves memory while attenuating age- related biomarker alterations n preclinical Alzheimer’s disease.
Every 67 seconds someone is diagnosed with AD in the United States, and in December 2017, the journal Alzheimer's and dementia reported that 46.7 million Americans had preclinical AD (amyloidosis, neurodegeneration, or both), although many may not progress to clinical disease during their lifetimes. Individuals with neurocognitive deficits therefore need to be screened for multiple causes of inflammation on the 16 point MSIDS map (see Chapter 2, Table 2.1: Symptoms and Associated Medical Conditions on the Sixteen-Point MSIDS Map) if we are to stem the tide of rising rates of chronic neurological disease and disability in the US.
Posted by Dr H, not representing the views of the Federal TBDWG.
http://www.sciencedirect.com/…/article/pii/S1877959X17305678
Abstract:
We report the case of an 80-year-old patient with acute onset confusion initially suspected to reflect delirium in incipient Alzheimer's disease. Cerebrospinal fluid tests revealed an unusually severe form of neuroborreliosis, which resolved following antibiotic treatment. This was mirrored in the measurement of CXCL13, which is suggested as a complementary biomarker"
What is CXCL13 and how does it relate to other inflammatory molecules in the body that are produced during an infection? Here is an explanation from "How Can I Get Better?" Chapter 3, Lyme Disease Specifics and Treatment Options:
"Scientific research has shown that borrelia creates an inflammatory response in the body where molecules are produced, called inflammatory cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF- alpha), and interferon gamma. These can cause fatigue,
pain, headaches, memory and concentration problems, and mood swings. Specialized signaling proteins, called chemokines, such as CCL-2 and CXCL-13, are also produced during an infection. These proteins recruit specialized immune cells such as B cells to make antibodies at the site of the infection, including the central nervous system, during neuroinflammation. Cytokines and chemokines can both modulate immune
activation and inflammation as they direct immune cells to the sites of tissue injury and infection".
"The reason that alternative diagnostic techniques are necessary to diagnose neuroborreliosis is that MRI’s, SPECT scans and PET scans of the brain are not able to definitively determine if a patient has neurological Lyme disease. Physicians will therefore occasionally perform a spinal tap and look at markers in the spinal fluid to determine if Borrelia burgdorferi has invaded the CNS. Unfortunately, spinal taps also have their limitations. Although increased antibody production in the spinal fluid can be seen in early Lyme disease with a lymphocytic meningitis or encephalitis, in late stage neurological Lyme patients, patients can have normal cerebrospinal fluid (CSF) antibody studies. For example, Dr. Coyle and Dr. Schutzer studied 35 patients with specific Lyme Antigen (Osp A) in their cerebrospinal fluid, indicative of neurological Lyme disease. Of these patients studied, although the Lyme antigen was positive, 43% had no evidence of antibodies to Lyme in their CSF testing, and 47% had otherwise normal routine CSF analyses. 60% of these patients were also seronegative for Lyme disease when tested with standard blood tests, implying that a patient can have Lyme disease despite a negative blood test and a negative spinal tap. The authors concluded that, “neurologic infection by B. burgdorferi should not be excluded solely on the basis of normal routine CSF or negative CSF antibody analyses.”
• Coyle PK, Schutzer SE, Deng Z, Krupp LB, Belman AL, Benach JL, Luft BJ. Detection of Borrelia burgdorferi-specific antigen in antibody-negative cerebrospinal fluid in neurologic Lyme disease. Neurology. 1995 Nov;45(11):2010-5;
Patients may also be seronegative for Lyme disease because of sequestration of antibody in immune complexes.
• Schutzer SE, Coyle PK, Belman AL, Golightly MG, Drulle J. Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease. Lancet. 1990 Feb 10;335(8685):312-5;
In Chapter 13 of "How Can I Get Better? I discuss nine factors on the Horowitz Sixteen-Point MSIDS Map, which have all been published in the scientific literature in the past several years, that have been proven to be associated with Alzheimer’s disease, apart from genetic influences. These factors are affecting the neurocognitive functioning of large numbers of the general population. They include
1. Multiple infections (Borrelia burgdorferi, other spirochetes (B.
miyamotoi, denticola spirochetes in the mouth); similar spiral shaped organisms (Helicobacter pylori); Chlamydia pneumonia; Porphyromonas gingivalis; viruses (HSV-1, cytomegalovirus); and possibly fungal infections;
2. Immune Dysfunction/Autoimmunity: Brain-reactive autoantibodies
3. Inflammation: The Framingham Study found inflammation
and an increase in inflammatory cytokines to increase the risk of
Alzheimer’s disease.
4. Environmental Toxins and Neuroimmunotoxicology: In 2014,
JAMA Neurology reported that levels of the pesticide DDE were
3.8- fold higher in those with AD. Other environmental toxins like ozone and small- particulate matter have also been linked to Alzheimer’s dementia.
5. Diet: Lipid- based diets effectively combat Alzheimer’s disease in the mouse model, and increases in dietary intake of either flavonoids (blueberries) or the omega-3 FA (DHA) in fish enhances neurogenesis and memory.
6. Sleep disorders: Lack of sleep contributes to elevations in
inflammatory cytokines like IL-6, & microinfarcts in the brain
7. Hormonal Dysregulation: Numerous studies have documented
a strong association between diabetes and Alzheimer’s disease
and suggest that avoiding excess insulin may help prevent and
lessen the impact of the disease.
8. Rest and Restore: Meditation may reduce hippocampal- volume atrophy in mild cognitive impairment (MCI), while having a positive impact on brain regions most related to dementia.
9. Exercise: increases the size of the hippocampus and improves memory while attenuating age- related biomarker alterations n preclinical Alzheimer’s disease.
Every 67 seconds someone is diagnosed with AD in the United States, and in December 2017, the journal Alzheimer's and dementia reported that 46.7 million Americans had preclinical AD (amyloidosis, neurodegeneration, or both), although many may not progress to clinical disease during their lifetimes. Individuals with neurocognitive deficits therefore need to be screened for multiple causes of inflammation on the 16 point MSIDS map (see Chapter 2, Table 2.1: Symptoms and Associated Medical Conditions on the Sixteen-Point MSIDS Map) if we are to stem the tide of rising rates of chronic neurological disease and disability in the US.
Posted by Dr H, not representing the views of the Federal TBDWG.
http://www.sciencedirect.com/…/article/pii/S1877959X17305678
