nCounter®
Alzheimer’s Disease Panel

Helping Your Research

Easily assess and monitor primary molecular characteristics of Alzheimer’s disease (AD) with standardized genes covering clinically-derived AD-associated modules. Now AD expression studies can be more reproducible and translationally relevant with an efficient workflow that potentially reduces the time to clinic. Reliably assay AD phenotypes and disease progression for mouse model development and human tissue screening.  

  • 770 genes specific to AD studies 
    • Comprehensive assessment of 30 AD-associated gene co-expression modules, including 23 neurodegeneration pathways and processes  
    • Reproducible monitoring of AD progression with age 
    • Functional screening of potential AD therapeutics   
  • Customizable with up to 55 additional user-defined genes with CodeSet Plus option
  • nCounter workflow is streamlined, user-friendly, and efficient, with just 15 minutes of total hands-on time 
  • Human and Mouse Panels available on-demand as a Custom CodeSet

Alzheimers Disease

How It Works

The content included in the nCounter AD panels represent a transcriptomic fingerprint of AD-related changes that can be directly compared to studies of mouse models of disease and back to human tissue. These panels allow for:

01:

Pathway Based Module Analysis

02:

Pathway Analysis

03:

Normalization

04:

Quality Control

05:

Differential Expression

06:

Gene Set Analysis

Panel Selection Tool

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

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Product Information

Product Specifications
Functional Annotations
Catalog Information
Product Specifications
Functional Annotations

† Annotations for 23 fundamental pathways and processes were assigned across all genes in the Mouse AD and Human AD panel allowing for an additional view of important aspects of the onset and progression of neurodegenerative disease. Pathways and processes with >60% representative gene content per module are listed above. 

‡ <60% representative pathway and process gene content per module. 

* Genes selected based on human-mouse gene homology, maximal coverage of AMP-AD modules, top AGORA candidate gene status (agora.ampadportal.org), representation in AMP-AD module eigengenes, and expression in mouse brain. 

Catalog Information

Related Resources

See All Resources
Product Bulletin Mouse and Human AD Panels- Product Bulletin
Blog Post A Systematic Evaluation of Immune Response and Plaque Microenvironment Variation in Alzheimer’s Disease
Case Study Inflammation in Alzheimer’s – Case Study
Case Study Microglia and Alzheimer’s – Case Study
Blog Post New Biology-Driven Drug Discoveries Needed for Treating of Alzheimer’s

Publications

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Spatial Analysis of Neural Cell Proteomic Profiles Following Ischemic Stroke in Mice Using High-Plex Digital Spatial Profiling.

Stroke is ranked as the fifth leading cause of death and the leading cause of adult disability in the USA. The progression of neuronal damage after stroke is recognized to be a complex integration of glia, neurons, and the surrounding extracellular matrix, therefore potential treatments must target the detrimental effects created by these interactions.

Idelalisib inhibits experimental proliferative vitroretinopathy.

Proliferative vitreoretinopathy (PVR) is a fibrotic eye disease that develops after rhegmatogenous retinal detachment surgery and open-globe traumatic injury. Idelalisib is a specific inhibitor of phosphoinositide 3-kinase (PI3K) δ.

Combined MEK and JAK/STAT3 pathway inhibition effectively decreases SHH medulloblastoma tumor progression.

Medulloblastoma (MB) is the most common primary malignant pediatric brain cancer. We recently identified novel roles for the MEK/MAPK pathway in regulating human Sonic Hedgehog (SHH) MB tumorigenesis.

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