This assay is currently not available in New York state.
This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.
1 - 3 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
0.7 mL (Note: This volume does not allow for repeat testing.)
Red-top tube, gel-barrier tube
If a red-top tube is used, transfer separated serum to a plastic transport tube.
Assessing neuronal damage related to various neurodegenerative diseases
This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.
There are significant variations in measured serum NfL levels among different methods and labs. Care must be taken when interpreting results obtained in different studies.
Direct comparisons of absolute values can only be done on the same source fluid (plasma or serum).9
A rise in NfL is not specific for a specific disease factor and may be caused by both neurodegenerative diseases or a head impact during sports. Results should only be used in conjunction with other clinical information when evaluating patients with neurodegeneration. Due to a lack of specificity to a particular neurodegenerative disease, its role as a diagnostic marker is limited.
There are numerous demographic, life style, and comorbidity factors that potentially influence NfL levels in serum. Variables such as exercise,76 blood volume, body mass index may impact measured serum NfL levels.
NfL levels measured in the morning are more than 10% higher than those measured in the evening.11,77
Caution should be taken in interpreting NfL levels when disease treatment induced neurological complications that can potentially impact NfL levels.28,78
Serum NfL levels can be decreased in patients with high immunoglobulin G (IgG) levels.
Roche Diagnostics Electrochemiluminescence Immunoassay (ECLIA)
0 to 4 y
5 to 9 y
10 to 14 y
15 to 19 y
20 to 29 y
30 to 39 y
40 to 49 y
50 to 59 y
60 to 69 y
70 to 79 y
Neurofilament proteins are protein polymers measuring 10 nm in diameter and many micrometers in length that, together with microtubules and microfilaments, form the neuronal cytoskeleton.1,2 These proteins are also prominent components of abnormal intra-neuronal aggregates in varied neurodegenerative diseases, including multiple sclerosis (MS), Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD) and Huntington disease (HD).3 Neurofilament light chain (NfL) is constantly released from neurons into the extracellular space and ultimately reaches the cerebrospinal fluid (CSF) under physiological conditions. CSF NfL concentrations can increase in neurodegeneration and neuronal injury across a wide range of neurologic diseases. Serum NfL (sNfL) levels in healthy individuals are about 2.5% of the levels in CSF and correlate highly with the concentrations in CSF.4-9 sNfL levels rise above normal in response to neuronal injury and neurodegeneration independent of cause.10
sNfL levels are increased in early relapsing multiple sclerosis (MS) and have been shown to correlate with markers of disease severity.4,11-20 In some reports, sNfL has been able to detect MS disease activity earlier than routine MRI21 and before clinical MS onset of disease.13,22,23 In patients with confirmed relapsing or progressive MS, sNfL can predict short-term outcomes including clinical and cognitive performance4,13,18,24 as well as predicting long-term worsening and risk of developing progressive MS.25 Treatment with disease modifying therapy has been reported to be associated with lower sNfL levels compared to untreated individuals.4,13,14,21,26,27 Increased sNfL levels can indicate neurotoxicity after hematopoietic stem cell transplant in multiple sclerosis.28
The application of sNfL as a potential biomarker for Alzheimer's disease (AD) has been extensively investigated.3,5,29-36 sNfL levels have been shown to be higher in patients with mild cognitive impairment and patients with AD compared with healthy controls.37,38 Moreover, higher sNfL levels have been associated with cognitive decline in non-dementia older adults.39 Elevated NfL levels have been associated with the presence of amyloid-beta plaques in pre-symptomatic individuals and with the load of tau in symptomatic patients.33 Increased sNfL levels have also been associated with AD progression independent of amyloid-beta.40 sNfL levels have been shown to correlate with Braak staging in AD41 and normal sNfL levels have been linked with resistance to PS1 familial AD in apolipoprotein E3 (APOE3) Christchurch mutation.42
In amyotrophic lateral sclerosis (ALS), elevated sNfL levels have been observed up to 3.5 years before symptom onset with the extent to which the elevation of NfL occurs prior to symptoms related to the specific gene mutation causing the disease.43,44 Levels of NfL have been shown to have excellent diagnostic and prognostic performance for symptomatic patients with ALS.45-49
sNfL levels reflect cortical neurodegeneration from the very early stages of Parkinson's disease (PD) and have been shown to track the underlying pathological process leading to PD dementia.12,50-56 Higher baseline NfL levels were also associated with greater motor and cognitive decline after a follow-up period of 3 years in patients with PD.12,51,52 sNfL levels correlated with disease severity and levels reflect cortical neurodegeneration from the very early stages of PD.51 In advanced PD patients, sNfL concentrations are associated with motor function, cognitive decline and subclinical cardiac damage.57
In HD, sNfL levels were significantly higher in patients than in healthy controls and significantly higher in manifest HD than pre-manifest HD.58-60 Increased sNfL levels were found in young adult carriers of HD gene mutation approximately 24 years before the clinical onset of symptoms.61
In frontotemporal dementia (FD), sNfL levels were found to be significantly higher than in healthy controls with the elevations correlating with disease severity.62 Increased sNfL levels were observed 1 to 2 years before the clinical onset of symptoms in patients with FD.63 In patients diagnosed with dementia with Lewy bodies (DLB), sNfL levels were found to be about 2-fold higher than in healthy controls with the elevations correlating with disease severity.64 sNfL levels were found to be a superior predictor of cognitive decline compared to age, sex and baseline severity variables in DLB.64 In patients with Charcot-Marie-Tooth neuropathy, sNfL levels were about 2-fold higher in patients than in healthy controls and levels correlated with disease severity.65-67 sNfL levels were also found to be significantly elevated in acquired peripheral neuropathy with levels that correlated not only with disease severity but also with outcome.68 sNfL levels also declined with remission.69
Increased levels of sNfL have been reported in patients with traumatic brain injury (TBI).70-74 sNfL levels are higher in all patients suffering from concussion compared to healthy controls. Sports-related concussion has specifically been associated with higher levels of sNfL.74
In the acute and post-acute phase after stroke, high sNfL levels are associated with poor clinical outcome and positively correlate with secondary neurodegeneration as assessed by MRI.75
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|140455||Neurofilament Light Chain||140456||Neurofilament Light Chain||pg/mL||Pending|
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