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nCounter®
Alzheimer’s Disease Panel

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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 for 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 Panel Plus option 
  • nCounter workflow is streamlined, user-friendly, and efficient with just 15 minutes total hands-on time 
  • Human Panel available off the shelf and Mouse Panel 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

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Normalization

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Quality Control

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Differential Expression

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Gene Set Analysis

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Built-in compatibility for Panel Plus and Protein analysis

Panel Selection Tool

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

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Product Information

Functional Annotations
Product Specifications
Catalog Information
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. 

Product Specifications
Catalog Information

Related Resources

See All Resources
Product Bulletin Mouse and Human AD Panels- Product Bulletin
Blog 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 New Biology-Driven Drug Discoveries Needed for Treating of Alzheimer’s

Publications

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Co-activation of Sonic hedgehog and Wnt signaling in murine retinal precursor cells drives ocular lesions with features of intraocular medulloepithelioma.

Intraocular medulloepithelioma (IO-MEPL) is a rare embryonal ocular neoplasm, prevalently occurring in children. IO-MEPLs share histomorphological features with CNS embryonal tumors with multilayered rosettes (ETMRs), referred to as intracranial medulloepitheliomas.

Characterization of the therapeutic effect of antibodies targeting the Ebola glycoprotein using a novel BSL2-compliant rVSVΔG-EBOV-GP infection model.

Ebola virus (EBOV) infections cause haemorrhagic fever, multi-organ failure and death, and survivors can experience neurological sequelae. Licensing of monoclonal antibodies targeting EBOV glycoprotein (EBOV-GP) improved its prognosis, however, this treatment is primarily effective during early stages of disease and its effectiveness in reducing neurological sequela remains unknown.

MMP9 Differentially Regulates Proteins Involved in Actin Polymerization and Cell Migration during TGF-β-Induced EMT in the Lens.

Fibrotic cataracts have been attributed to transforming growth factor-beta (TGF-β)-induced epithelial-to-mesenchymal transition (EMT). Using mouse knockout (KO) models, our laboratory has identified MMP9 as a crucial protein in the TGF-β-induced EMT process.

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