The Neural ZoomerTM is an array of neurological autoantibodies which offers very specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM is designed to assess an individual’s reactivity to neurological antigens, which may have connections to a variety of neurologically related diseases.
With a panel of 16 of the most well-studied neurological autoantibodies, the Neural ZoomerTM is able to guide providers in treatment protocols by pinpointing the mechanisms behind disease progression and providing a roadmap to solutions and improved health outcomes in this challenging arena of disease.
The test also has optional additional genetic testing for the ApoE genotype, which has been shown to influence risk for certain neurological conditions.
The Vibrant Neural ZoomerTM aims to reduce the prevalence of neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.
By including the Vibrant Neural ZoomerTM in their arsenal of available autoimmune and neurological tests, healthcare providers can arm themselves with the most advanced and relevant test available to assess the presence and risk of neurological autoimmunity.
The Neural ZoomerTM is also the comprehensive compilation of multiple research studies which have identified autoantibodies associated with a range of neurological disorders, enabling early risk detection and prevention of neurological degeneration.
The Vibrant Neural ZoomerTM includes a comprehensive set of autoimmune markers, from a single serum draw including:
- Anti-tubulin lgM/lgG+lgA
- Anti-myelin basic protein lgM/lgG+lgA
BLOOD BRAIN BARRIER DISRUPTION
- Anti s100b lgM/lgG+lgA
OPTICAL AND AUTONOMIC NERVOUS SYSTEM DISORDER
- Anti-neuron specific enolase lgM/lgG+lgA
- Anti-GM1 lgM/lgG+lgA
- Anti-GM2 lgM/lgG+lgA
- Anti-HSV1 lgM/lgG+lgA
- Anti-cerebellum lgM/lgG+lgA
- Anti-purkinje cell lgM/lgG+lgA
(Available upon request)
- Apolipoprotein E
Symptoms associated with autoimmunity in the nervous system include:
- Sensory loss
- Impaired vision
- Muscle pain/spasms
- Muscle weakness/atrophy
- Orthostatic hypotension
- Chronic pain/fibromyalgia
- Memory loss or brain fog
- Autoimmune disease
Can I use the Neural ZoomerTM in the pediatric population?
It is important to note that Vibrant Neural ZoomerTM has been validated in the adult population only. While we encourage and utilize this test in pediatric patients, there is a potential for false negatives in this population, as the reference ranges are established for adults.
A child’s immune system develops over time. They may not have “mature enough” immunoglobulins to mount a significant antibody response. Pediatric reference ranges for total immunoglobulin IgA, IgG, and IgM are much lower than adult reference ranges. Positive/reactive antigens on a pediatric test does indicate sensitivity, but a non-reactive test in the pediatric population could potentially be a false negative. In other words, there is a possibility that the Neural ZoomerTM test may not discover a child’s immune response to those neurological antigens tested. It is important to assess a pediatrics baseline immunoglobulin response by measuring total immunoglobulins. Total IgG and total IgA are available on the Vibrant Wheat ZoomerTM. Despite this potential limitation, many of our practitioners use the Wheat ZoomerTM in pediatric populations regularly.
How are reference ranges for the Vibrant Neural ZoomerTMdetermined?
Vibrant has given a numerical value to quantify the antibodies measured by chemiluminescent signal of our microchip. The determination of the positive cutoff is by 97.5 percentile of 192 normal healthy controls. If you are above 97.5 percentile, you are considered positive. If 5% below cutoff (92.5-97.5 percentile), results are borderline. Less than 92.5 percentile, results are negative.
Should I do this test if I have had a concussion previously?
Yes! Post-concussion or traumatic brain injury (TBI) is a good reason to run this test. The Vibrant Neural ZoomerTM measures markers of blood brain barrier permeability (s100B antibodies) that are associated with disruption to the blood brain barrier (BBB), which can often occur after concussion or TBI. The Neural ZoomerTM can show an increase in anti-neuron specific enolase antibodies, which are associated with optical neuropathies or traumatic brain injury (TBI).
When should I run the Neural ZoomerTM on a patient?
Anyone with symptoms of autoimmunity in the nervous system, such as neuropathic pain, MS, ataxia, brain fog, memory loss, etc, would benefit from the Neural ZoomerTM. Because many of these conditions are related to celiac, and wheat and gluten enteropathies, it is best run after a Wheat ZoomerTM to check for intestinal permeability as well celiac and wheat/gluten sensitivity.
Anti Tubulin Tamara Vyshkina and Bernadette Kalman. “Autoantibodies and neurodegeneration in multiple sclerosis.
The Study shows the role of anti-tubulin antibodies in the development of inflammatory demyelination and neurodegeneration in patients carrying LHON mtDNA mutations.
Connolly AM, Pestronk A. “Anti-tubulin autoantibodies in acquired demyelinating polyneuropathies.
Analysis of 7 human sera with monoclonal anti-tubulin autoantibodies showed that the epitopes recognized by
these antibodies are within central, conserved regions of tubulin. Selective polyclonal anti-tubulin autoantibodies with low reactivity to other neural antigens are found in about one-half of patients with Chromic inflammatory demyelinating polyneuropathy.
Anti Myelin basic protein
Berger T, Rubner P, Schautzer F, Egg R, Ulmer H, Mayringer I, Dilitz E, Deisenhammer F, Reindl M.Antimyelin antibodies as a predictor of clinically definite multiple sclerosis after a first demyelinating event
A total of 103 patients with a clinically isolated syndrome, positive findings on cerebral MRI, and oligoclonal bands in the cerebrospinal fluid were studied. At base line, serum samples were collected to test for anti-MOG and anti-MBP antibodies with Western blot analysis, and the lesions detected by cerebral MRI were quantified.Patients with anti-MOG and anti-MBP antibodies had relapses more often and earlier than patients
without these antibodies. The adjusted hazard ratio for the development of clinically definite multiple sclerosis
was 76.5 for both antibodies
de Rosbo NK, Ben-Nun A. “T-cell responses to myelin antigens in multiple sclerosis; relevance of the predominant autoimmune reactivity to myelin oligodendrocyte glycoprotein
High titres of anti-MOG autoantibodies have been detected in paediatric patients with a variety of demyelinating inflammatory diseases.
Blood Brain barrier
disruption Anti s100b – blood brain barrier Erin Bargerstock,et. al. “Is Peripheral Immunity Regulated by Blood-Brain Barrier Permeability Changes?
Extravasation of S100B into the systemic circulation can r a pathologic autoimmune reaction with circulating antibodies that may re-enter the CNS to initiate an autoimmune response . S100B can be viewed as an astrocytic endokine that can act as an immunoregulator to participate in inflammation and autoimmunity.
Dyck RH, Van Eldik LJ, Cynader MS. “Immunohistochemical localization of the S-100 beta protein in postnatal cat visual cortex: spatial and temporal patterns of expression in cortical and subcortical glia.
S-100 is primarily synthesized in the brain by the end feet process of the astrocytes and is quickly released from
the brain in the blood when the BBB is disrupted.
Optical and Autonomic
Nervous System Disorders Anti Neuron specific enolase Ikeda Y, Maruyama I, Nakazawa M, Ohguro H.Clinical significance of serum antibody against neuron specific enolase in glaucoma patients.
Serum autoantibody against NSE was examined by Western blot analysis in 143 patients with glaucoma 45 cases; primary open angle glaucoma (POAG) 98 cases.Maximum IOP in the serum anti-NSE antibody-positive patients was significantly lower than that in the negative patients. The current observation suggest that the presence of serum autoantibody against NSE clinically useful for predicting the progression of visual field loss in POAG patients.
Grazyna Adamus, Lori Brown, Jade Schiffman,and Alessandro Iannaccone. Diversity in autoimmunity against retinal, neuronal, and axonal antigens in acquired neuroretinopathy.
209 patients (whose visual disorders were due to autoimmune in nature) were tested for anti-optic nerve autoantibodies, 55% showed specific neuronal autoantibodies among which 25% seropostive patients showed high levels and enolases Autoantibodies.
Ogino M, Orazio N, Latov N.IgG anti-GM1 antibodies from patients with acute motor neuropathy are predominantly of the IgG1 and IgG3 subclasses.
In this study, the IgG anti-GM1 and GA1 antibodies from patients with acute motor neuropathy were predominantly IgG1 and IgG3.
Lee GH1, Lee KW, Chi JG.Peripheral neuropathy as a hypereosinophilic syndrome and anti-GM1 antibodies.
The authors experienced a dramatic case with acute peripheral neuropathy, hypereosinophilia in peripheral blood, and the positive anti-GM1 antibodies.
Hugh J. Willison, Nobuhiro Yuki. “Peripheral neuropathies and antiglycolipid antibodies.
The review article discuss the understanding between acute motor axonal neuropathy and antibodies to GM1, GD1a,
GM1b and GalNAc-GD1a, and between the cranial, bulbar and sensory variants of GBS and antibodies to the disialylated gangliosides GQ1b, GT1a, GD1b and GD3.
O’Hanlon GM, Veitch J, Gallardo E, Illa I, Chancellor AM, Willison HJ. Peripheral neuropathy associated with antiGM2 ganglioside antibodies: clinical and immunopathological studies.
AntiGM2 antibodies are found in cases of chronic motor or motor dominant neuropathy. In this study, two chronic neuropathy cases were identified with highly elevated antiGM2 IgM titres.
Anti-Cerebellum,Paula Goines, Lori Haapanen, Robert Boyce et.al. “Autoantibodies to cerebellum in children with autism associate with behavior
Results autoantibodies specific for a 45kDa cerebellar protein in children were associated with a diagnosis of autism (p=0.017) while autoantibodies directed towards a 62kDa protein were associated with the broader diagnosis of autism spectrum disorder (ASD) (p=0.043).
Luc Letenneur ,KarinePérès, Hervé Fleury, Isabelle Garrigue, Pascale Barberger-Gateau, Catherine Helmer, Jean-Marc Orgogozo, Serge Gauthier, Jean-François Dartigues Seropositivity to Herpes Simplex Virus Antibodies and Risk of Alzheimer’s Disease: A Population-Based Cohort Study
The authors describe the reactivation of HSV seropositivity which is highly correlated with incident AD. IgM-positive subjects showed a significant higher risk of developing AD (HR=2.55; 95% CI [1.38–4.72]).
S. Jarius and B. Wildemann “‘Medusa head ataxia’: the expanding spectrum of Purkinje cell antibodies
in autoimmune cerebellar ataxia. Part 1: Anti-mGluR1, anti-Homer-3, anti-Sj/ITPR1 and anti-CARP VIII
This review article discusses the role of the antigens in spinocerebellar ataxia and focuses specifically on antimetabotropic glutamate receptor 1-, anti-Homer protein homolog 3-, and anti-carbonic anhydrase-related protein VIII-associated autoimmune cerebellar ataxia (ACA)
Chia-Chen Liu, TakahisaKanekiyo, Huaxi Xu, and Guojun Bu. “Apolipoprotein E and Alzheimer disease:risk, mechanisms, and therapy.
Genome-wide association studies have confirmed that the ε4 allele of APOE is the strongest genetic risk factor for AD. The frequency of AD and mean age at clinical onset are 91% and 68 years of age in ε4 homozygotes, 47% and 76 years of age in ε4 heterozygotes, and 20% and 84 years in ε4 noncarriers,7, 20 indicating that APOE ε4 confers dramatically increased risk of development of AD with an earlier age of onset in a gene dose-dependent manner.
Farrer LA et.al. “Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium.
Among Caucasian subjects from clinic- or autopsy-based studies, the risk of AD was significantly increased for
people with genotypes ε2/ε4 (OR=2.6, 95% CI=1.6-4.0), ε3/ε4 (OR=3.2, 95% CI=2.8-3.8), and ε4/ε4 (OR=14.9,95% CI= 10.8-20.6); whereas, the ORs were decreased for people with genotypes ε2/ε2 (OR=0.6, 95% CI=0.2-2.0) and ε2/ε3 (OR=0.6, 95% CI=0.5-0.8).