nCounter®
Neuropathology Panel

Helping Your Research

Biomarker discovery and signature development are essential for identification of novel therapies and for earlier detection and development of therapies for neurodegenerative disorders like Alzheimer’s Disease (AD), Parkinson’s Disease (PD), and Amyotrophic Lateral Sclerosis (ALS). The nCounter Neuropathology Panel helps perform comprehensive multiplex gene expression analysis in human or mouse samples with genes involved in six fundamental themes of neurodegeneration: neurotransmission, neuron-glia interaction, neuroplasticity, cell structure integrity, neuroinflammation, and metabolism.

  • Developed for research of Alzheimer’s Disease, Parkinson’s Disease, Amyotrophic Lateral Sclerosis, Frontotemporal Dementia, Huntington’s Disease, and other neurological disorders
  • Includes unique cell typing feature for measuring the abundance of five important CNS cell types, including neurons, astrocytes, microglia, oligodendrocytes, and endothelial cells
Neuropathology Panel

How It Works

nCounter Neuropathology Panels utilize NanoString’s unique barcoding technology and the nCounter Analysis System to help accelerate your research.

01:

Screen 770 genes specific for neurodegeneration

02:

Comprehensively Assess 23 pathways

03:

Monitor progression of neurodegeneration

04:

Screen potential therapeutics

05:

Discover biomarkers and develop signatures associated with neurodegeneration

06:

Customize with up to 55 additional user-defined genes with the Panel Plus option

07:

Get data quickly with a streamlined, user-friendly, and efficient workflow with only 15 minutes hands-on time

Panel Selection Tool

Find the gene expression panel for your research with easy to use panel pro

Find Your Panel

Product Information

CNS Cell Typing
Functional Annotations
Product Specifications
Catalog Information
CNS Cell Typing

Genes included in the Neuropathology Panels provide unique cell profiling data for measuring the abundance1 of five important cell types including neurons, astrocytes, microglia, oligodendrocytes, and endothelial cells. The table below summarizes each cell type represented in the panels along with the gene content qualified through current literature references.

1Danaher P. et al. Gene expression markers of Tumor Infiltrating Leukocytes JITC 2017

Functional Annotations

Functional annotations for 23 fundamental pathways and processes were assigned across all genes in the Neuropathology Panels allowing for a practical view of important aspects of the onset and progression of neurodegenerative disease.

Product Specifications
Catalog Information

Related Resources

See All Resources
Product Bulletin nCounter Neuroinflammation Panel – Product Bulletin
Whitepaper Neuro Pub Review – Whitepaper
Blog Post Advancing Neuroscience Gene Expression Research
App Note/Tech Note Deciphering complexities of neurodegeneration and neuroinflammation
Blog Post Of Inflammasome and Tauopathies in Mice and Men

Publications

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A single-cell atlas of glioblastoma evolution under therapy reveals cell-intrinsic and cell-extrinsic therapeutic targets.

Recent longitudinal studies of glioblastoma (GBM) have demonstrated a lack of apparent selection pressure for specific DNA mutations in recurrent disease. Single-cell lineage tracing has shown that GBM cells possess a high degree of plasticity.

INPP5D deficiency attenuates amyloid pathology in a mouse model of Alzheimer’s disease.

Introduction: Inositol polyphosphate-5-phosphatase (INPP5D) is a microglia-enriched lipid phosphatase in the central nervous system. A non-coding variant (rs35349669) in INPP5D increases the risk for Alzheimer’s disease (AD), and elevated INPP5D expression is associated with increased plaque deposition.

Signatures for Viral Infection and Inflammation in the Proximal Olfactory System in Familial Alzheimer’s Disease.

Alzheimer’s disease (AD) is characterized by deficits in olfaction and olfactory pathology preceding diagnosis of dementia. Here we analyzed differential gene and protein expression in the olfactory bulb (OB) and tract (OT) of familial AD (FAD) individuals carrying the autosomal dominant presenilin 1 E280A mutation.

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