
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 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

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Product Information
† 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.
Related Resources






Publications
Retrospective Validation of a 168-Gene Expression Signature for Glioma Classification on a Single Molecule Counting Platform.
Gene expression profiling has been shown to be comparable to other molecular methods for glioma classification. We sought to validate a gene-expression based glioma classification method.
Supratentorial ependymoma in childhood: more than just RELA or YAP.
Two distinct genetically defined entities of ependymoma arising in the supratentorial compartment are characterized by the presence of either a C11orf95-RELA or a YAP-MAMLD1 fusion, respectively. There is growing evidence that supratentorial ependymomas without these genetic features exist.
Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits.
Background: Disruptions of brain-gut axis have been implicated in the progression of a variety of gastrointestinal (GI) disorders and central nervous system (CNS) diseases and injuries, including traumatic brain injury (TBI). TBI is a chronic disease process characterized by persistent secondary injury processes which can be exacerbated by subsequent challenges.

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