Quinolinate is a neurotoxin derived from tryptophan. Elevated quinolinate is seen in brain and nerve tissue damage, especially in disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, motor neuron diseases, multiple sclerosis, epilepsy, amyotrophic lateral sclerosis, and major depressive disorder. We can also see elevated quinolinate due to low serotonin and need for vitamin B3 (niacin). The causes of elevated quinolinate include neuroinflammation, general inflammation, infection, phthalate exposure, and/or oral tryptophan use.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Tryptophan and its different pathways:

The management of tryptophan converting to serotonin within the brain has some complex moving parts. Tryptophan gets converted into serotonin. High levels of stress of any type and acute/chronic infections can change this process by provoking an immune system response. Instead of serotonin being made from tryptophan in this process, two other compounds are eventually made: They are kynurenic acid which is neuroprotective and quinolinic acid which is neurodegenerative.The quinolinic acid is a NMDA-agonist, i.e. quinolinic acid, NMDA, and inflammation are best friends and like to wreak havoc when kynurenic acid is lacking. Recent research showed that patients suffering from severe depression and suicidality were found to have very high levels of inflammation and elevated NMDA activity as a result of long-term dysregulation of this pathway. The researchers’ recommended goal was to find ways to dampen the NMDA receptors and quinolinic acid in the brain.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Quinolinate is a neurotoxin derived from tryptophan. Elevated quinolinate is seen in brain and nerve tissue damage, especially in disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, motor neuron diseases, multiple sclerosis, epilepsy, amyotrophic lateral sclerosis, and major depressive disorder. We can also see elevated quinolinate due to low serotonin and need for vitamin B3 (niacin). The causes of elevated quinolinate include neuroinflammation, general inflammation, infection, phthalate exposure, and/or oral tryptophan use.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

A high ratio of quinolinic acid to the tryptophan metabolite, 5-hydroxyindoleacetic acid, indicates excessive inflammation due to recurrent infections, excessive tryptophan intake, immune overstimulation, excessive adrenal production of cortisol, or excessive exposure to phthalates.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

A high ratio of quinolinic acid to the tryptophan metabolite, 5-hydroxyindoleacetic acid, indicates excessive inflammation due to recurrent infections, excessive tryptophan intake, immune overstimulation, excessive adrenal production of cortisol, or excessive exposure to phthalates.

A high ratio of quinolinic acid to the tryptophan metabolite, 5-hydroxyindoleacetic acid, indicates excessive inflammation due to recurrent infections, excessive tryptophan intake, immune overstimulation, excessive adrenal production of cortisol, or excessive exposure to phthalates.

The R. rickettsii IFA - IgG marker on a Rickettsiosis panel is a crucial diagnostic tool for identifying infection with Rickettsia rickettsii, the bacterium responsible for Rocky Mountain spotted fever (RMSF), a potentially severe tick-borne illness. This serological test detects Immunoglobulin G (IgG) antibodies that the immune system produces specifically in response to an R. rickettsii infection. IgG antibodies are part of the body's later immune response, typically developing a few weeks after initial exposure to the pathogen and potentially persisting for years, thus indicating either past exposure or chronic infection.

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An "Indeterminate" result (if result falls in orange reference range) in the R. rickettsii IFA - IgG test indicates that the detected levels of IgG antibodies against Rickettsia rickettsii, the causative agent of Rocky Mountain spotted fever (RMSF), are unclear and do not conclusively fall within the defined positive or negative ranges. This ambiguous result can be due to several reasons. It might suggest that the antibody levels are at a borderline range, possibly indicating an early immune response where the antibodies are just starting to develop and have not reached a level high enough to be considered positive. Alternatively, it could be a sign of declining antibody levels from a past infection that is resolving or has already resolved, where the antibodies are present but at diminishing levels. An indeterminate result can also arise from technical issues in the test procedure or cross-reactivity with antibodies from other similar infections. In such cases, further evaluation is necessary, often including a clinical assessment of symptoms, patient history, and possibly additional diagnostic tests, such as a repeat IgG test after some time or other serological tests like IgM testing. This indeterminate outcome highlights the complexity of diagnosing RMSF based solely on serological testing and underscores the importance of a comprehensive clinical assessment to accurately determine the infection status.

The R. typhi IFA - IgG marker on a Rickettsiosis panel is a specialized diagnostic tool used for the detection of IgG antibodies against Rickettsia typhi, the causative agent of murine typhus. This serological assay plays a critical role in the diagnosis of the disease, particularly in epidemiological settings where murine typhus is prevalent. IgG antibodies are a key component of the adaptive immune response, typically developing within a few weeks following exposure to a pathogen and persisting for an extended period, thereby indicating past exposure or a possible chronic infection.

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An "Indeterminate" result (a result that falls within the orange reference range) in the R. typhi IFA - IgG test signifies that the levels of IgG antibodies against Rickettsia typhi, the bacterium responsible for murine typhus, are ambiguous and do not clearly fall into the positive or negative categories. This uncertain result can occur for several reasons. It may indicate that the antibody levels are at a borderline, possibly suggesting an early stage of the immune response where antibodies are just starting to develop but haven't reached a definitive positive level. Alternatively, it could be a sign of declining antibody levels from a past infection that is resolving or has already resolved, where the antibodies are present but at diminishing levels. Technical factors within the test itself or cross-reactivity with antibodies from other similar pathogens can also contribute to an indeterminate result. In such cases, further evaluation is often necessary, including a clinical assessment of symptoms, patient history, and possibly additional diagnostic tests, such as a repeat IgG test after some time or IgM testing. This indeterminate outcome emphasizes the need for a comprehensive approach in diagnosing murine typhus, considering serological results alongside the broader clinical picture to accurately determine the infection status.

The rheumatoid arthritis (RA) latex turbid test is a laboratory test that’s used to help your doctor diagnose rheumatoid arthritis and other autoimmune diseases.