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
Transcriptional profiling of paediatric ependymomas identifies prognostically significant groups.
The majority of supratentorial ependymomas in children contain oncogenic fusions, such as ZFTA-RELA or YAP1-MAMLD1. In contrast, posterior fossa (PF) ependymomas lack recurrent somatic mutations and are classified based on gene expression or methylation profiling into group A (PFA) and group B (PFB).
Absence of CD28-CTLA4-PD-L1 Costimulatory Molecules Reduces Herpes Simplex Virus 1 Reactivation.
We previously reported that herpes simplex virus 1 (HSV-1) ICP22 binds to CD80 and suppresses CD80 expression in vitro and in vivo. Similar to ICP22, the cellular costimulatory molecules CD28, CTLA4, and PD-L1 also bind to CD80.
Chronic complement dysregulation drives neuroinflammation after traumatic brain injury: a transcriptomic study.
Activation of the complement system propagates neuroinflammation and brain damage early and chronically after traumatic brain injury (TBI). The complement system is complex and comprises more than 50 components, many of which remain to be characterized in the normal and injured brain.
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