Olink Explore 384 Neurology Ⅱ Panel

What is the Olink Explore 384 Neurology Ⅱ Panel 

Customized panel for human

The Olink Explore 384 Neurology II Panel employs Proximity Extension Assay (PEA) methodology to simultaneously measure 367 neural biomarkers using just 1 μL of plasma or serum, processing 88 samples per analytical run. This advanced platform demonstrates exceptional detection capability (<1 pg/mL) and inter-assay consistency (<5% coefficient of variation) through Normalized Protein Expression (NPX) data standardization. Featuring a flexible architecture with eight distinct biomarker subpanels, the system supports both expansive neurological profiling and hypothesis-driven investigations, while maintaining rigorous quality assurance through National Institute of Standards and Technology (NIST)-traceable reference materials for dependable biomarker identification.

Features of the pane

• Species: Validated for human proteome studies only.
• Proteins: 384 neural biomarkers analyzed simultaneously.
• Sample: 1 µL plasma/serum input.
• Readout: Normalized Protein Expression (NPX) quantitative values.
• Platform: Designed specifically for Olink Signature Q100 platform.

List of 384 human derived biomarkers

Protein category

The Olink Explore 384 Neurology II Panel enables comprehensive profiling of 367 carefully curated proteins organized into eight functionally distinct categories: neural cell adhesion and guidance molecules, neurotrophic factors and their receptors, synaptic proteins and regulators, neuroinflammatory mediators, extracellular matrix and structural components, enzymatic and metabolic regulators, growth factor modulators, along with other functionally relevant proteins (see Table. List of Olink Explore 384 Neurology Ⅱ Panel). Expert neuroscientists selected these targets based on their established involvement in critical neural processes, including development, axonal guidance, and synaptic plasticity, as well as their relevance to neurological conditions like Alzheimer's. All included biomarkers, particularly low-abundance analytes, have undergone rigorous validation assessing analytical performance across multiple parameters: sample compatibility, target specificity, measurement precision, detection sensitivity, dynamic range capability, matrix interference resistance, and potential cross-reactivity.

Protein Functions

Biological process

Central to immune system operations, axon guidance regulation, and developmental biology systems

Disease area

Associated with metabolic regulation, neurological function, and developmental processes.

The Application of Olink Explore 384 Neurology ⅡPanel.

The Olink Explore 384 NeurologyⅡ Panel allows for the parallel measurement of 384 protein biomarkers linked to neurological pathways, offering researchers a robust solution for:

• Quantitative assessment of barrier integrity markers (adhesion molecules, transporters);
• Monitoring of neurovascular unit communication pathways;
• Discovery of novel signaling molecules in barrier dysfunction models;
• Multi-omics integration for comprehensive barrier function analysis. 

Workflow of Olink Proteomics

Why CPR

Enhanced Neurology Biomarker Coverage

Expands to 384 carefully curated protein targets, including novel markers for synaptic plasticity, neuroinflammation, and neurodegeneration.

Pre-Configured Neuroscience Workflows

Optimized analytical pipelines for Alzheimer's, Parkinson's, and ALS research, incorporating validated biomarker ratios and neural pathway mapping.

Customizable Research Panels

Allocates 42 flexible slots for user-defined targets while retaining core neurology biomarkers.

Collaborative Panel Design

Offers co-development of study-specific assays with Olink's scientific team, ensuring target relevance.

Demo Results of Olink Data

Volcano map of individual proteins associated with inflammatory bowel disease and its subtypes in the UK Biobank. (Xuening Zhang., et al. 2025)

Sample Requirements

Case Study

Corticotropin-releasing hormone as a candidate biomarker for parkinsonian disorders

Journal: Brain Commun
Year: 2024

• Background
• Methods
• Results

Patients with Parkinsonism (PS) need disease-specific fluid biomarkers. Adrenocorticotropin-releasing hormone (CRH) is considered a biomarker of Lewy body disease. Therefore, this study aims to confirm CRH as a potential biomarker for different PS. We assay CRH and misfolded α-synuclein (αSyn) in CSF.

Using Olink Explore 3072, we analyzed the CSF proteomic profiles of two independent Swedish cohorts using proximity extension assays. αSyn aggregation was assessed using SAA (SAA- vs. SAA+). The Biomarkers for Identifying Neurodegenerative Disorders Early and Reliably 2 (BioFINDER-2) trial cohort included 632 participants, comprising 317 individuals with unimpaired cognitive function (CUI), 37 SAA+ CUIs, and 77 patients with SAA+ Lewy body disease (Parkinson's disease = 46; dementia with Lewy bodies = 31), 37 (SAA− = 35; SAA+ = 2) with atypical PS [PSP = 25 (SAA−= 23; SAA+ = 2); MSA = 12 (SAA−= 12; SAA+ = 0)], and 164 patients with non-Parkinsonian neurodegenerative diseases (SAA−= 120, SAA+ = 44). A validation cohort (BioFINDER-1) included 143 patients, consisting of 58 SAA- CUIs, 27 SAA+ Lewy body disease patients (Parkinson's disease = 25; Parkinson's disease dementia = 1; Lewy body dementia = 1), and 58 atypical PS [PSP = 28 (SAA−= 26; SAA+ = 1; NA = 1); MSA = 30 (SAA−= 20; SAA+ = 6); cerebrospinal fluid CRH was compared between the two groups and correlated with motor, cognitive, psychiatric, and cerebrospinal fluid inflammatory markers.

In the BioFINDER-2 study, CSF CRH was reduced in SAA Lewy and SAA CUI individuals compared with SAA-CUI individuals had a similar reduction in CRH compared to SAA Lewy's body disease (Figure 1B). Researchers also evaluated CRH in non-Lewy body diseases, including Alzheimer's disease/frontotemporal dementia/vascular dementia and atypical PS (Figure 1D). Due to frequent αSyn copathology in Alzheimer's disease, Researchers only compared SAA-Alzheimer's disease/frontotemporal dementia/vascular dementia individuals with SAA Lewy body disease. Researchers found that CRH expression was downregulated in SAA Lewy body disease compared to SAA-Alzheimer's disease/frontotemporal dementia/vascular dementia. When comparing SAA- with SAA Alzheimer's disease/frontotemporal dementia/vascular dementia, researchers found no difference in CRH levels. Among them, atypical PS individuals [PSP = 25 (SAA−= 23; Saa = 2); Msa = 12 (saa−= 12; SAA = 0 compared to SAA−CUI group), and down-regulation was stronger in the CRH group (Fig. 1E) than in the Lewy body disease group. To ensure that the downregulation of CRH in atypical PS was not affected by MSA or PSP alone, researchers made separate comparisons. Researchers found that CRH was reduced for both PSP and MSA compared to SAA−CUI (Figures 1F and G). Exclusion of two SAA atypical PS individuals did not affect the results.

Figure 1 Levels of corticotropin-releasing hormone measured in cerebrospinal fluid samples from BioFINDER-2 cohort participants. (Fernandes Gomes, B. et al. 2024)

FAQs

References

1. Zhang, X., Zhao, H., Wan, M., et al. (2025). Associations of 2923 plasma proteins with incident inflammatory bowel disease in a prospective cohort study and genetic analysis. Nature communications, 16(1), 2813. https://doi.org/10.1038/s41467-025-57879-3 
2. Fernandes Gomes, B., Kumar, A., Ashton, N. J., et al. (2024). Corticotropin-releasing hormone as a candidate biomarker for parkinsonian disorders. Brain communications, 6(6), fcae414. https://doi.org/10.1093/braincomms/fcae414