Neurofascin (NF) is a cell adhesion molecule (= cell adhesion molecules are transmembrane glycoproteins that enable cells to bind together and attach to the extracellular matrix).

NF is expressed in both the CNS and the peripheral nervous system (PNS) and plays important roles in developing and maintaining neural structures.

Anti-neurofascin autoantibodies are found mainly in combined central and peripheral demyelination (CCPD), a rare demyelinating condition affecting both CNS and peripheral nervous system (PNS) tissues, and also in chronic inflammatory demyelinating polyneuropathy (CIDP) and axonal injury in patients with multiple sclerosis (MS). Recognition of this antibody may be important in treatment management, becauseanti-neurofascin seropositive CCPD patients respond well to Intravenous Immunoglobulin or plasma exchange treatments.

Neurofascin (NF) is a cell adhesion molecule (= cell adhesion molecules are transmembrane glycoproteins that enable cells to bind together and attach to the extracellular matrix).

NF is expressed in both the CNS and the peripheral nervous system (PNS) and plays important roles in developing and maintaining neural structures.

Anti-neurofascin autoantibodies are found mainly in combined central and peripheral demyelination (CCPD), a rare demyelinating condition affecting both CNS and peripheral nervous system (PNS) tissues, and also in chronic inflammatory demyelinating polyneuropathy (CIDP) and axonal injury in patients with multiple sclerosis (MS). Recognition of this antibody may be important in treatment management, becauseanti-neurofascin seropositive CCPD patients respond well to Intravenous Immunoglobulin or plasma exchange treatments.

Neuron specific enolase is a protein enzyme that is encoded by the ENO2 gene. It is found in mature neurons and cells of neuronal origin. Antibodies against neuron specific enolase are found in patients with optical neuropathies (= damage inflicted on the optic nerve in your eye).

Neuron specific enolase is a protein enzyme that is encoded by the ENO2 gene. It is found in mature neurons and cells of neuronal origin. Antibodies against neuron specific enolase are found in patients with optical neuropathies (= damage inflicted on the optic nerve in your eye).

Anti-Nuclear Antibody by IFA (RDL) refers to a diagnostic test that detects antinuclear antibodies (ANAs) in the blood. ANAs are a group of autoantibodies that target substances found in the nucleus of cells, and their presence is often associated with various autoimmune disorders.

The IFA, or Indirect Fluorescent Antibody method, is a common technique used for this test. It involves adding a patient's serum to a substrate containing cells, and then, if ANAs are present, they bind to the nuclei in the cells. After washing away unbound antibodies, a fluorescent-labeled secondary antibody is added, which attaches to any bound ANAs. Under a fluorescence microscope, the presence of ANAs is indicated by a specific pattern of fluorescence in the cells' nuclei.

This test is particularly important in diagnosing conditions like systemic lupus erythematosus, Sjögren's syndrome, scleroderma, and mixed connective tissue disease.

Antibodies against proteinase 3 (PR3) are referred to as c-ANCA fluorescent subtype, namely cytoplasmic antibodies (granular cytoplasmic fluorescence). PR3 is a neutral serine proteinase 3, also known as Wegener's autoantigen. Antibodies against PR3 are a highly specific marker in diagnosing Wegener's granulomatosis.

Purkinje cells, or Purkinje neurons, are a class of GABAergic neurons located in the cerebellum. Purkinje cells are aligned like dominos stacked one in front of the other. Their large dendritic arbors form nearly two-dimensional layers through which parallel fibers from the deeper-layers pass.

What It Measures

The test detects IgG and IgA antibodies targeting Purkinje cells, the primary inhibitory neurons in the cerebellum, responsible for motor coordination and cognitive processing. These antibodies may bind to intracellular or membrane-associated proteins, such as ARHGAP26 (linked to cerebellar ataxia) or Yo antigens (e.g., CDR2/CDR2L in paraneoplastic syndromes).

Clinical Relevance

Anti-Purkinje cell antibodies are associated with:

• Paraneoplastic Cerebellar Degeneration (PCD):

  • Strongly linked to underlying cancers (e.g., breast, ovarian, or lung malignancies), with 90-98% of anti-Yo-positive cases having neoplasms.

  • Symptoms include subacute cerebellar ataxia, dysarthria, and diplopia.

• Autoimmune Cerebellar Ataxia:

  • Non-paraneoplastic cases often target antigens like ARHGAP26 or RGS8, causing inflammatory cerebellar damage.

• Psychiatric and Neurodevelopmental Disorders:

  • Anti-Purkinje antibodies (IgG) are reported in schizophrenia, bipolar disorder, and ADHD, correlating with acute psychopathology and positive symptoms.

  • May disrupt cerebellar-limbic circuits involved in emotion and cognition.

The Anti-Purkinje cell (IgM) marker on Vibrant America’s Neural Zoomer Plus panel detects IgM-class autoantibodies targeting Purkinje cells, specialized neurons in the cerebellum that are critical for motor coordination. This test is part of a broader evaluation for neurological autoimmunity, helping identify immune-mediated damage linked to conditions like cerebellar ataxia, paraneoplastic syndromes, or neurodegenerative disorders.

What is Anti-RAGE Peptide?

The Anti-RAGE peptide (IgG + IgA) marker measures the presence of antibodies against the Receptor for Advanced Glycation End Products (RAGE) in the blood. This receptor plays a crucial role in inflammation, immune system regulation, and neural function. RAGE is highly expressed in the brain, particularly in neurons, microglia, and endothelial cells of the blood-brain barrier.

Moderately Elevated Anti-RAGE Peptide (IgG + IgA) – What Does It Mean?

A moderate elevation in Anti-RAGE Peptide (IgG + IgA) on the Neural Zoomer Plus panel suggests an ongoing but not severe immune response against the Receptor for Advanced Glycation End Products (RAGE). This may indicate low-grade neuroinflammation, early-stage neurological dysfunction, or an autoimmune process that is not yet fully developed.

Possible Implications of a Moderate Elevation:

1. Early or Mild Neuroinflammation

   • The immune system is reacting to RAGE, but the inflammatory response is not yet severe.
   • This could be associated with brain fog, mild cognitive dysfunction, headaches, or early neurodegenerative changes.

2. Blood-Brain Barrier Disruption (Mild to Moderate)

   • RAGE plays a role in blood-brain barrier (BBB) integrity.
   • A moderate increase in anti-RAGE antibodies may indicate some permeability changes, allowing unwanted substances or immune cells to cross into the brain.

3. Metabolic & Glycation-Related Stress

   • RAGE interacts with advanced glycation end products (AGEs), which accumulate in conditions like insulin resistance, diabetes, and oxidative stress.
   • A moderate elevation might be a sign of subclinical metabolic dysfunction rather than an overt disease process.

4. Autoimmune Activity – Subclinical or Developing

   • A moderately elevated result may be an early indicator of autoimmune activity, particularly in conditions like multiple sclerosis (MS), lupus (SLE), or rheumatoid arthritis.
   • However, without other strongly positive markers, it may suggest a transient immune activation rather than an established autoimmune disease.

5. Chronic Low-Grade Infection or Environmental Trigger

   • Mild elevations can occur due to persistent infections, chronic stress, gut dysbiosis, or environmental toxins that subtly activate the immune system over time.

What Should You Do If Moderately Elevated?

• Monitor Symptoms: Pay attention to changes in cognitive function, mood, energy levels, or neurological symptoms.
• Assess Inflammation & Oxidative Stress: Consider testing CRP, homocysteine, oxidative stress markers, and metabolic health to evaluate systemic inflammation.
• Support the Blood-Brain Barrier & Nervous System:
  • Anti-inflammatory diet (reduce processed foods, refined sugars, and AGEs from overcooked/fried foods).
  • Gut-brain support (probiotics, glutathione, polyphenols).
  • Antioxidants (curcumin, resveratrol, alpha-lipoic acid).
• Address Potential Triggers: Investigate toxic exposures (mold, heavy metals, pesticides), chronic infections, and immune dysfunction.
• Follow-Up Testing: If symptoms progress, consider re-testing anti-RAGE antibodies and other neural immune markers over time.

Bottom Line:

A moderately elevated Anti-RAGE Peptide (IgG + IgA) result is not necessarily pathological but may indicate early neuroinflammatory activity, metabolic stress, or mild blood-brain barrier disruption. It is important to monitor changes, manage inflammation, and identify possible contributing factors to prevent progression toward neurodegeneration or autoimmune disease.

Anti recoverin antibodies are one of the key components of antibody disorders of the central nervous system (CNS). They have also been shown to be associated with retinopathy, which is characterized by impaired vision and photosensitivity.