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
- Human Panel available off the shelf and Mouse Panel available on-demand as a Custom CodeSet
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:
Pathway Based Module Analysis
Gene Set Analysis
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 proFind Your Panel
† 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.
The bidirectional lung brain-axis of amyloid-β pathology: ozone dysregulates the peri-plaque microenvironment.
The mechanisms underlying how urban air pollution affects Alzheimer’s disease (AD) are largely unknown. Ozone (O3) is a reactive gas component of air pollution linked to increased AD risk, but is confined to the respiratory tract after inhalation, implicating the peripheral immune response to air pollution in AD neuropathology.
Intratarget Microdosing for Deep Phenotyping of Multiple Drug Effects in the Live Brain.
A main impediment to effective development of new therapeutics for central nervous system disorders, and for the in vivo testing of biological hypotheses in the brain, is the ability to rapidly measure the effect of novel agents and treatment combinations on the pathophysiology of native brain tissue. We have developed a miniaturized implantable microdevice (IMD) platform, optimized for direct stereotactic insertion into the brain, which enables the simultaneous measurement of multiple drug effects on the native brain tissue in situ.
Differential protein expression in the hippocampi of resilient individuals identified by digital spatial profiling.
Clinical symptoms correlate with underlying neurodegenerative changes in the vast majority of people. However, an intriguing group of individuals demonstrate neuropathologic changes consistent with Alzheimer disease (AD) yet remain cognitively normal (termed “resilient”).