nCounter® Neuroinflammation Panel
Helping Your Research
Neuroinflammation research today requires a broad view of all the underlying aspects of neurological disorders and injury, including an assessment of neurotransmission, neuron-glia interactions, neuroplasticity, cell integrity, neuroinflammation, and metabolism. The nCounter Neuroinflammation Panels support and simplify your neuroinflammation research needs by providing a complete view of the complex interplay between the immune system and the Central Nervous System (CNS). These panels deliver a comprehensive evaluation of the pathways, processes, and cell types that are involved in neuroinflammation. Product highlights include:
- Gene expression profiling of neuroimmune interactions
- The study of drug treatment response and signature generation
- Biomarker characterization
- Research of neurodegenerative disease, traumatic brain injury, psychiatric disorders, neuropathic pain, CNS infection, and others
How It Works
The Neuroinflammation Panels are based on the nCounter barcoding technology that allows for direct quantification of hundreds of transcripts with an automated platform that requires minimal hands-on time. Complete your projects in record time by spending less time on sample prep and more time getting insights from data that can be analyzed in minutes with the nSolver™ Analysis Software or ROSALIND. These panels include 770 genes for human and mouse studies on inflammation of the CNS.
Comprehensively assess 23 neuroinflammation pathways and processes
Measure the relative abundance of 5 CNS cell types and 14 peripheral immune cell types with the unique cell profiling feature
Customizable with Panel Plus option – add up to 55 genes of your choice
Use only 15 minutes hands-on time to set up the streamlined, user-friendly, and efficient nCounter workflow
Panel Selection Tool
Find the gene expression panel for your research with easy to use panel proFind Your Panel
Genes included in the Neuroinflammation Panels provide unique cell profiling data for measuring the relative abundance of 5 CNS and 14 peripheral immune cell types in a single sample1. The table below summarizes each cell type represented by gene content in the panel qualified through biostatistical approaches and selected literature in the field of neuroinflammation research.
1Danaher P. et al. Gene expression markers of Tumor Infiltrating Leukocytes JITC 2017
Functional annotations for 23 pathways and processes were assigned across the genes in the Neuroinflammation Panels. The 23 pathways and processes represent three core themes of neuroinflammation: immunity and inflammation, neurobiology and neuropathology, and metabolism and stress.
The role of innate immunity in many neurological disorders is now widely accepted in the research world although the relative contributions of these processes to the progression and/or amelioration of these diseases is incompletely understood. Several key processes and pathways are assessed in this panel to provide a comprehensive view of the immune and inflammatory response in the nervous system.
Neuropathology research today requires a broad view of all the underlying aspects of neurological disorders and injury, including an assessment of neurotransmission, neuron-glia interactions, neuroplasticity, cell integrity, neuroinflammation, and metabolism. There are 13 pathways and processes included in this panel to evaluate the impact of neuroinflammation and immune actions in the nervous system on neuropathology.
Metabolic dysfunction and stress have been shown to influence brain activity and disrupt CNS homeostasis and cognitive function by adopting neurotoxic functions. The genes selected for this panel are designed to assess important aspects of metabolism and stress that are known to impact neuroinflammation.
Transcriptional profiling of paediatric ependymomas identifies prognostically significant groups.
The majority of supratentorial ependymomas in children contain oncogenic fusions, such as ZFTA-RELA or YAP1-MAMLD1. In contrast, posterior fossa (PF) ependymomas lack recurrent somatic mutations and are classified based on gene expression or methylation profiling into group A (PFA) and group B (PFB).
Absence of CD28-CTLA4-PD-L1 Costimulatory Molecules Reduces Herpes Simplex Virus 1 Reactivation.
We previously reported that herpes simplex virus 1 (HSV-1) ICP22 binds to CD80 and suppresses CD80 expression in vitro and in vivo. Similar to ICP22, the cellular costimulatory molecules CD28, CTLA4, and PD-L1 also bind to CD80.
Chronic complement dysregulation drives neuroinflammation after traumatic brain injury: a transcriptomic study.
Activation of the complement system propagates neuroinflammation and brain damage early and chronically after traumatic brain injury (TBI). The complement system is complex and comprises more than 50 components, many of which remain to be characterized in the normal and injured brain.