Preclinical WebsiteClinical Website

Explore this Service: 

What Services does Biospective offer for Neurofilament Light Chain (NF-L) Analysis?

Neurofilament light chain (NF-L) is a neuron-specific cytoskeletal protein released into the extracellular fluid (ECF) following axonal damage or neurodegeneration. Elevated NF-L levels serve as a highly sensitive biomarker for neuronal injury & damage, offering translational value for preclinical and clinical research.

What Different Sample Types are Supported for Neurofilament Light Chain (NF-L) Analysis?

Sample Types Supported

Our assays support NF-L quantification in multiple biofluids and biological matrices, allowing flexibility in experimental design across in vivo and in vitro systems:

 

Blood (Plasma, Serum)

  • Minimally invasive, ideal for longitudinal studies
  • Clinically accessible and translationally relevant

Cerebrospinal Fluid (CSF)

  • Gold-standard for central nervous system (CNS) biomarker analysis
  • Directly reflects neurodegeneration and neuronal/axonal injury

Cell Culture Media

  • Enables NF-L monitoring in neuronal and co-culture systems
  • Supports screening of disease-modifying therapeutics, neurotoxic compounds, genetic modifications, or inflammatory responses

Sample Collection, Preparation, and Shipping Guidelines

We provide comprehensive support to ensure sample integrity and data reliability

  • Sample Collection: Blood and CSF samples should be collected using standard aseptic techniques.
  • Sample Preparation: Blood and CSF samples should be centrifuged, aliquoted, and frozen at -80°C.  Cell culture media should be centrifuged before freezing at -80°C.
  • Sample Shipping: Samples should be shipped on dry ice using insulated containers, avoiding repeated freeze-thaw cycles.

Neurofilament light chain (NF-L) is released from injured/damaged axons into the extracellular space and subsequently can be detected in CSF and blood.

What is Neurofilament Light Chain (NF-L)?

NF-L is a key structural protein within neuronal axons, forming part of the neurofilament triplet (NF-L, NF-M, and NF-H). Axonal damage or injury from disease, trauma, or toxicity leads to NF-L release into CSF and blood, where it can be measured as a quantitative, non-invasive biomarker of neuronal integrity.


Why Measure NF-L? 

  • Non-invasive biomarker of neuronal damage
  • Tracks disease progression and therapeutic efficacy
  • Applicable across multiple neurological and neurodegenerative diseases and conditions, including: 
    • Amyotrophic Lateral Sclerosis (ALS)
    • Multiple Sclerosis (MS)
    • Alzheimer's Disease
    • Parkinson's Disease
    • Tauopathies (FTD, Progressive Supranuclear Palsy, Corticobasal Degeneration)
    • Huntington's Disease
    • Spinocerebellar Ataxias
    • Traumatic Brain Injury (TBI) & Concussion

Explore how NF-L, the ultrasensitive neurofilament immunoassay, and key rodent models - including EAE and rNLS8 - are used to study neurodegeneration, monitor disease progression, and evaluate potential therapies. This video provides a clear overview of each tool and its translational relevance for preclinical research.

How is Neurofilament Light Chain (NF-L) Measured in Biological Fluids?

Advanced NF-L immunoassays, such as Ella™ (Simple Plex™, ProteinSimple™, Bio-Techne®), Meso Scale Discovery (MSD), and Simoa® (Quanterix) enable detection of NF-Light in diverse biological matrices with high accuracy and precision.

Comparison of Commonly Used Platforms for NF-L Analysis

Feature

Ella™
(Bio-Techne®) 

MSD
(Meso Scale Discovery)

Simoa®
(Quanterix) 

 Assay Type 

 Microfluidic immunoassay

 Electrochemiluminescence (ECL) immunoassay

 Digital ELISA (single molecule array)

Time to Results

~90 minutes

4 - 6 hours

3 - 4 hours

Automation

Fully-automated

Semi-automated

Fully-automated

Sample Types

Plasma
Serum
CSF
Cell culture media
Tissue homogenate supernatants

Plasma
Serum
CSF
Cell culture media
Tissue homogenate supernatants

Plasma
Serum
CSF
Cell culture media
Tissue homogenate supernatants

Throughput / Format

Up to 72 samples/run
with triplicate measurements

Up to 40 samples/run
with duplicate measurements

Up to 40 samples/run
with duplicate measurements

This table compares three NF-L assay platforms - Bio-Techne Ella™, MSD, and Quanterix Simoa® -  across key criteria, including assay type, time to results, level of automation, supported sample types, and throughput per run.

What is the Value of Neurofilament Light Chain (NF-L) in Animal Models?

Preclinical Applications

NF-L is widely used in animal models to monitor neurodegeneration and/or axonal injury, disease progression, and therapeutic efficacy. Our validated platforms and experience enable robust NF-L quantification across multiple model systems.

Multiple Sclerosis (MS) Models

In human MS, NF-L is a sensitive and reliable biomarker for monitoring disease progression and treatment response (Ferreria-Atuesta, 2021). Elevated NF-L levels indicate heightened relapse risk and disease activity, while effective disease-modifying therapies reduce NF-L concentrations  (Freedman, 2025).

EAE Model (Experimental Autoimmune Encephalomyelitis) of MS

Mimics autoimmune-mediated MS-like pathology, including: 

  • Neuroinflammation
  • Peripheral inflammatory infiltrates
  • Demyelination in white matter tracts
  • Axonal injury/damage & axon degeneration

NF-L serves as a quantitative biomarker of CNS demyelination and axonal injury.

For more on this model, see our Resources:

Plots of NF-L in blood and CSF from the EAE model of MS

Plasma and CSF NF-L data comparing EAE to Sham controls; mean ± SEM.

Amyotrophic Lateral Sclerosis (ALS) Models

NF-L is an emerging biomarker of neuroaxonal damage in ALS. In patients, NF-L concentrations are elevated in both CSF and blood, correlating with disease severity, rate of progression, and survival (Anjum, 2025). Beyond reflecting neuronal injury, NF-L shows promise as a prognostic marker capable of distinguishing clinically relevant patient subgroups (Krishnamurthy, 2024). 

TDP-43ΔNLS (rNLS8) Model of ALS

At Biospective, we use both the original and modified versions of the rNLS8 ALS mouse model of TDP-43 proteinopathy.

  • Original mouse model ("Off Dox"): rapidly progressing (weeks)
  • Biospective mouse model ("Low Dox"): slower progression (months) 

TDP-43ΔNLS models exhibit progressive: 

NF-L quantification provides a non-invasive measure of disease progression and treatment response.

For more information, see our Resources:

In the "Image Interactive" below, you can explore the relationship between increased NF-L levels and pathologic changes shown on high-resolution Multiplex Immunofluorescence tissue sections from Biospective's “Low Dox” TDP-43ΔNLS (rNLS8) mouse model.

In the Image Viewer, you can pan around the image using the left mouse button. You can zoom in and out using the mouse/trackpad (up/down) or the + and - buttons in the upper left corner. You can toggle (on/off), change color, and adjust image settings for the channels in the Control Panel in the upper right corner.

We suggest using Full Screen Mode for the best interactive experience.

NF-L Quantification in the TDP-43ΔNLS Mouse Model of ALS

1/5

https://ispproductionpublic.blob.core.windows.net/media/1e7a4868-236a-40a9-9d44-23d2a0c3437e/1e7a4868-236a-40a9-9d44-23d2a0c3437e

This “Image Interactive” Story highlights neurofilament light chain (NF-L) data from Biospective’s TDP-43ΔNLS (rNLS8) mouse model of ALS and relates it to the pathologic changes observed in these mice.

Both the original (“Off Dox”) and Biospective’s (“Low Dox”) models exhibit characteristic TDP-43 mislocalization, motor deficits, neuroinflammation, and neurodegeneration. NF-L quantification provides a sensitive, non-invasive biomarker of axonal degeneration and neurodegenerative disease progression across both models.

The accompanying multiplex immunofluorescence (mIF) images from the Low Dox model were generated by immunostaining for hTDP-43, GFAP, Iba-1, and counterstained with the DAPI nuclear stain.

To navigate though this Image Story, you can use the arrows and/or the Table of Contents icon in the upper right corner of this panel.

https://ispproductionpublic.blob.core.windows.net/media/a61d8ef6-9c45-4c94-80f5-e30100747aab/a61d8ef6-9c45-4c94-80f5-e30100747aab

You can also interact with the microscopy image in the viewer on the right at any time to further explore this high-resolution data.

NF-L in Amyotrophic Lateral Sclerosis (ALS)

Neurofilament light chain (NF-L) is a well-established biomarker of axonal/neuronal degeneration in ALS. A pathologic hallmark of ALS is mislocalization of TDP-43 from the nucleus to the cytoplasm. This characteristic cytoplasmic mislocalization can be replicated in animal models, such as Biospective’s TDP-43ΔNLS Low Dox mouse model (see microscopy image in the Image Viewer).

In patients, NF-L levels in both CSF and blood correlate with disease severity, rate of progression, and survival (Anjum, 2025). NF-L is, therefore, widely recognized as a translational biomarker bridging preclinical and clinical ALS research.

CSF NF-L in the TDP-43ΔNLS (rNLS8) Mouse Model of ALS

In Biospective’s TDP-43ΔNLS (rNLS8) mouse models, NF-L levels were quantified under different doxycycline (Dox) treatment conditions. These models vary in the degree of transgene expression and in their rates of disease progression.

The graphs below present CSF NF-L concentrations measured in On Dox (control), Low Dox, and Off Dox mice.

CSF NF-L concentrations in On Dox vs. Low Dox TDP-43ΔNLS mice.

CSF NF-L concentrations in On Dox vs. Low Dox TDP-43ΔNLS mice. ****p<0.0001

CSF NF-L concentrations in On Dox vs. Off Dox TDP-43ΔNLS mice.

CSF NF-L concentrations in On Dox vs. Off Dox TDP-43ΔNLS mice. ****p<0.0001.

This microscopy image shows reactive astrocytes. Neuroinflammation in this model is presumed to be associated with the process of active neurodegeneration which leads to the release of NF-L into the extracellular space.

Measures of NF-L in the blood and CSF can be complemented by in vivo MRI measures of brain atrophy (an imaging biomarker of neurodegeneration). Together, this multi-modality biomarker approach provides high sensitivity and specificity for analyzing neurodegenerative changes.

Cortical thinning map highlights regions of cortical thinning in Low Dox mice compared with controls. Green and yellow areas indicate significant thinning, which corresponds to the astrogliosis observed in the multiplex immunofluorescence image.

Plasma NF-L in the TDP-43ΔNLS (rNLS8) Mouse Model of ALS

The graphs below show plasma NF-L concentrations in On Dox (control), Low Dox, and Off Dox mice.

Plasma NF-L concentrations in On Dox vs. Low Dox TDP-43ΔNLS mice

Plasma NF-L concentrations in On Dox vs. Low Dox TDP-43ΔNLS mice. ****p<0.0001.

Plasma NF-L concentrations in On Dox vs. Off Dox TDP-43ΔNLS mice

Plasma NF-L concentrations in On Dox vs. Off Dox TDP-43ΔNLS mice. ****p<0.0001.

This microscopy image illustrates neuroinflammatory interactions between microglia and neurons, a phenotype observed in this model. When these interactions become dysregulated, they can contribute to pathological synaptic elimination and neurodegeneration, thereby resulting in increased release of NF-L from the neurons. In this image, the arrow highlights contact points between the neuronal soma and microglial processes.

Summary

Both CSF and plasma NF-L concentrations increase with reduced Dox levels, consistent with greater transgene expression and faster disease progression in the TDP-43ΔNLS model. These findings demonstrate clear, measurable differences in NF-L across treatment conditions and highlight its value as a sensitive translational biomarker.

When integrated with complementary readouts, such as MRI measures of brain atrophy and multiplex immunofluorescence markers of neuroinflammation, NF-L serves as a robust endpoint for characterizing neurodegeneration in the TDP-43ΔNLS model.

https://ispproductionpublic.blob.core.windows.net/media/1e7a4868-236a-40a9-9d44-23d2a0c3437e/1e7a4868-236a-40a9-9d44-23d2a0c3437e

Table of Contents
Control Panel
Section: Coronal Brain
Channels

Increased NF-L levels and pathologic changes shown on high-resolution Multiplex Immunofluorescence tissue sections from Biospective's “Low Dox” TDP-43ΔNLS (rNLS8) mouse model

Parkinson's Disease Models

In PD patients, NF-L concentrations are increased relative to healthy controls, and have been reported to correlate with clinical measures of disease severity and progression (Pilotto, 2021; Ou, 2024). Elevated NF-L levels in CSF and blood have also been shown to differentiate PD from atypical parkinsonian syndromes (Angelopoulou, 2021; Buhmann, 2023).

A plot of NF-L in blood and CSF from synuclein PFF mice

Plasma and CSF NF-L levels in M83+/- transgenic mice injected with recombinant human α-syn PFFs into the AON or MFB, compared to controls; mean ± SEM.

α-Synuclein PFF Model of PD

The α-synuclein preformed fibril (PFF) model reproduces key aspects of Parkinson's disease pathology and progression, making it a widely used tool for studying neurodegeneration and testing therapeutic interventions.

Key features of the α-syn PFF model include: 

  • Seeding and spreading of α-synuclein aggregates in a well-defined spatiotemporal pattern
  • Extensive α-synuclein pathology in neuronal cell bodies and neurites
  • Neuroinflammation (microgliosis & astrogliosis) and neurodegeneration

NF-L quantification in this model provides a readout of neurodegeneration.

For more details on NF-L analysis in this model, see our Resource:

A plot of NF-L in CSF from AAV-synuclein mice

CSF NF-L data comparing AAV-Syn to wild type (WT) controls; mean ± SEM.

AAV A53T α-Synuclein Model of PD

The AAV A53T α-synuclein model replicates key pathological features of human Parkinson's disease, including: 

  • Loss of dopaminergic neurons in the substantia nigra pars compacta
  • Dopaminergic denervation of the striatum
  • Aggregates of phosphorylated α-synuclein in cell bodies and neurites
  • Neuroinflammation (microgliosis & astrogliosis)
  • Motor dysfunction due to loss of dopaminergic innervation

NF-L quantification in the model provides a sensitive and quantifiable readout of neurodegeneration, supporting both mechanistic studies and therapeutic evaluation.

For more information on this model, see our Resource:

Alzheimer's Disease Models 

In patients with AD, both CSF and plasma NF-L concentrations are consistently linked to greater cognitive and overall clinical decline, underscoring the value of NF-L as a predictive biomarker for disease progression (Thomas, 2025). 

A plot of NF-L in CSF from APP/PS1 (ARTE10) mice

CSF NF-L data comparing female APP/PS1 (ARTE10) to wild type (WT) controls; mean ± SEM.

APP/PS1 (ARTE10) Transgenic Model of AD

Replicates Alzheimer's disease-like amyloid-beta pathology, including:

  • Progressive amyloid-β (Aβ) plaque deposition with time-dependent increases in burden and extent
  • Fibrillar extracellular and intracellular Aβ pathology
  • Dense core and diffuse plaques
  • Vascular Aβ pathology (cerebral amyloid angiopathy; CAA)
  • Neuroinflammation (microgliosis & astrogliosis)

NF-L quantification provides a sensitive biomarker of neurodegeneration in this model.  

For more on this model and our innovative analyses, see:

Ella™, Simple Plex™, ProteinSimple™, and Bio-Techne® are trademarks of Bio-Techne; Simoa® is a trademark of Quanterix.

To discuss your study requirements or request a quote for NF-L quantification services

Contact Us
FAQs

What is neurofilament light chain (NF-L)?

What sample types are supported for NF-L analysis at Biospective?

How is NF-L measured?

Which neurological or neurodegenerative diseases are associated with elevated NF-L?

Can NF-L predict disease progression?

Are complementary biomarker services available at Biospective?

References

Keywords

Related Content

Up-to-date information on Neurofilament Light Chain assays and services.

More Information

Let us know what you’re interested in. Our team will be happy to discuss with you!

Email us at i[email protected] or simply complete & submit the form below. 

Name*
Email*
Purpose of Inquiry*
Affiliation (Company/Institution)*
Message*

Your privacy is important to us. We will protect your data as outlined in our Privacy Notice.

I agree to the terms in the Privacy Notice*

We use necessary cookies to make our site work. We also use other cookies to help us make improvements by measuring how you use the site or for marketing purposes. You have the choice to accept or reject them all. For more detailed information about the cookies we use, see our Privacy Notice.