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Neuropathology Panel

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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

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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 Neuropathology Panel – Product Bulletin
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Flyer Custom Solutions Neuropathic Pain – Flyer
Blog Advancing Neuroscience Gene Expression Research

Publications

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Directly reprogrammed Huntington’s disease neural precursor cells generate striatal neurons exhibiting aggregates and impaired neuronal maturation.

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder characterized by the progressive loss of striatal medium spiny neurons. Using a highly efficient protocol for direct reprogramming of adult human fibroblasts with chemically modified mRNA, we report the first generation of HD induced neural precursor cells (iNPs) expressing striatal lineage markers that differentiated into DARPP32+ neurons from individuals with adult-onset HD (41-57 CAG).

Acute inflammatory profiles differ with sex and age after spinal cord injury.

BACKGROUND: Sex and age are emerging as influential variables that affect spinal cord injury (SCI) recovery. Despite a changing demographic towards older age at the time of SCI, the effects of sex or age on inflammation remain to be elucidated.

The degree of astrocyte activation is predictive of the incubation time to prion disease.

In neurodegenerative diseases including Alzheimer’s, Parkinson’s and prion diseases, astrocytes acquire disease-associated reactive phenotypes. With growing appreciation of their role in chronic neurodegeneration, the questions whether astrocytes lose their ability to perform homeostatic functions in the reactive states and whether the reactive phenotypes are neurotoxic or neuroprotective remain unsettled.

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