Glial Profiling Panel
Helping Your Research
Comprehensively study the role of astrocytes, microglia, and oligodendrocytes in health and disease with the nCounter Glial Profiling Panel. Decipher the complex interplay between glial cells, peripheral immune cells, and neurons that underlies neurodegenerative & neuroinflammatory disorders and neurotrauma such as stroke, spinal cord injury, and traumatic brain injury.
How It Works
The Glial Profiling panel covers comprehensive glial cell biology involved in both homeostasis and disease and can be run on its own or paired with the Neuropathology or Neuroinflammation panels.
Profile 770 human or mouse genes across 50+ pathways involved in glial cell biology:
- Cell stress & Damage Response
- Pathways Regulating Glia
- Inflammation & Peripheral Immune Invasion
- Glial Cell Homeostasis & Activation
Quantify the relative abundance of 5 CNS cell types and 14 peripheral immune cells
Customizable with Panel Plus option – add up to 55 genes of your choice
Panel Selection Tool
Find the gene expression panel for your research with easy to use panel proFind Your Panel
Directly reprogrammed Huntington’s disease neural precursor cells generate striatal neurons exhibiting aggregates and impaired neuronal maturation.
Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder characterized by the progressive loss of striatal medium spiny neurons. Using a highly efficient protocol for direct reprogramming of adult human fibroblasts with chemically modified mRNA, we report the first generation of HD induced neural precursor cells (iNPs) expressing striatal lineage markers that differentiated into DARPP32+ neurons from individuals with adult-onset HD (41-57 CAG).
Acute inflammatory profiles differ with sex and age after spinal cord injury.
BACKGROUND: Sex and age are emerging as influential variables that affect spinal cord injury (SCI) recovery. Despite a changing demographic towards older age at the time of SCI, the effects of sex or age on inflammation remain to be elucidated.
The degree of astrocyte activation is predictive of the incubation time to prion disease.
In neurodegenerative diseases including Alzheimer’s, Parkinson’s and prion diseases, astrocytes acquire disease-associated reactive phenotypes. With growing appreciation of their role in chronic neurodegeneration, the questions whether astrocytes lose their ability to perform homeostatic functions in the reactive states and whether the reactive phenotypes are neurotoxic or neuroprotective remain unsettled.