Longevity Brain Glial Blood Test

$410.00

Glial cells, often referred to as glia or neuroglia, are non-neuronal cells in the central nervous system (CNS) and peripheral nervous system (PNS) that do not produce electrical impulses. They are crucial for providing support and protection for neurons, the primary cells responsible for communication within the nervous system. Glial cells outnumber neurons by about ten to one, highlighting their importance in neural function. The main types of glial cells, each with distinct functions, include astrocytes, oligodendrocytes, microglia, and Schwann cells.

Currently, while there is no direct blood test that can measure microglial or overall glial activity in the brain with high specificity, glial activity can be indirectly inferred through blood biomarkers that indicate glial activation or neuroinflammation. This test measures some of those biomarkers.

Longevity Brain Blood Test: 18 Analytes tested: Brain-Derived Neurotrophic Factor (BDNF), C-Reactive Protein (CRP), Glial Fibrillary Acidic Protein (GFAP), Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Interleukin-10 (IL-10), Interferon-gamma (IFN-γ), Matrix Metalloproteinase 9 (MMP9), Neurofilament Light Chain (NfL), Soluble TREM2 (sTREM2), S100 Calcium-Binding Protein B (S100B), Tumor Necrosis Factor-alpha (TNF-α), Uric Acid, YKL-40 (Chitinase 3-like-1)

 

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Description

Currently, there is no direct blood test that can measure microglial or overall glial activity in the brain with high specificity. Glial cells, including microglia, astrocytes, oligodendrocytes, and Schwann cells, play crucial roles within the central and peripheral nervous systems, primarily localized within these areas. Their activities, such as neuroinflammation, support, and myelination, are critical for maintaining the nervous system’s health and responding to injury or disease. However, because these cells reside within the nervous system, their direct activity cannot be measured through blood tests in the same way some diseases or conditions can be. That being said, glial activity can be inferred indirectly through blood biomarkers that may indicate glial activation or neuroinflammation. This test measures some of these biomarkers.
Kynurenine Pathway of Tryptophan Metabolism and Neuroinflammation

Kynurenine Pathway of Tryptophan Metabolism and Neuroinflammation

The kynurenine pathway (KP) of tryptophan metabolism plays a crucial role in the balance between neuroprotection and neurotoxicity. Dysregulation of this pathway has been associated with several neurodegenerative and neuropsychiatric disorders, largely due to the potential role of KP metabolites in mediating neuroinflammation.

  1. Initiation of the Pathway: The metabolism of tryptophan via the kynurenine pathway begins with its conversion into kynurenine. This step is catalyzed by two primary enzymes: indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO). Both enzymes can be induced by pro-inflammatory stimuli, especially IDO, which is upregulated by pro-inflammatory cytokines like interferon-gamma (IFN-γ).
  2. Neuroactive Metabolites:
    1. Kynurenic Acid (KYNA): Produced in astrocytes, KYNA acts as an antagonist at NMDA and α7 nicotinic acetylcholine receptors. It has neuroprotective effects but, in elevated concentrations, might also contribute to cognitive dysfunctions.
    2. Quinolinic Acid (QUIN): This is synthesized in microglia and acts as an NMDA receptor agonist. Elevated levels can lead to excitotoxicity, which is damaging to neurons and is associated with several neurodegenerative conditions.
  3. Neuroinflammation: An imbalance favoring the production of QUIN over KYNA can contribute to neuroinflammation. QUIN’s agonistic action on NMDA receptors can lead to excitotoxic neuronal death. Moreover, QUIN can generate reactive oxygen species (ROS) and exacerbate inflammation. Chronic inflammation can upregulate IDO, leading to a sustained increase in kynurenine metabolites, which further skews the balance towards neurotoxic effects.
  4. Role in Neurodegenerative Diseases: Dysregulation of the kynurenine pathway is observed in various neurodegenerative conditions, including:
    1. Alzheimer’s Disease (AD): Elevated levels of QUIN and reduced KYNA levels have been reported in the brains of AD patients. QUIN can promote amyloid-beta aggregation, a hallmark of AD pathology.
    2. Parkinson’s Disease (PD): KP dysregulation is suggested to be involved in the dopaminergic neuronal loss characteristic of PD.
    3. Huntington’s Disease (HD): Elevated QUIN levels have been observed in the brains of HD patients and are believed to contribute to the striatal neurodegeneration seen in HD.
  5. Neuropsychiatric Implications: Changes in the KP have also been associated with neuropsychiatric disorders like depression, schizophrenia, and bipolar disorder. The balance between KYNA and QUIN can influence neurotransmission, synaptic plasticity, and neural integrity, potentially leading to mood and cognitive disturbances.

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Tests are not available to residents of New York. Any orders and/or samples originating from the state of New York will automatically be canceled. 

The information provided on this website is intended for educational purposes only and should not be considered as a substitute for professional medical advice, diagnosis, or treatment. It is essential to consult with your healthcare provider for any specific medical concerns or if you require medical advice, diagnosis, or treatment. Longevity Lab-Solutions tests may or may not alert you or your doctor to serious medical conditions and are not intended to replace an examination by your doctor. It is recommended to seek the advice of your healthcare professional for specific medical concerns.

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