Extract the most out of precious neuroscience samples
Neurodegeneration, neuroinflammation, infectious disease, and neurotrauma can have devastating effects on the Central Nervous System (CNS) that impact cognitive function, behavior, mental health, and more. Understanding the role of CNS cells such as neurons, astrocytes, glia, and oligodendrocytes as well as the pathways involved in disorders such as Alzheimer’s, Parkinson’s, Frontotemporal Dementia (FTD), Amyotrophic Lateral Sclerosis (ALS), and Multiple Sclerosis (MS) is crucial to disease prevention, detection, and treatment.
We know it’s difficult to acquire diseased and normal CNS tissue for research. When samples are available, extracting the most biological information from every experiment with a multi-omic platform that is easy to use is important. Traditional, low-plex methods of profiling RNA and protein such as PCR, western blotting, immunohistochemistry, or immunofluorescence staining provide limited information on CNS structure and functionality. RNA Sequencing, while more comprehensive for expression analysis, does not directly quantify transcripts, requires time-consuming, tedious steps and onerous data analysis and sacrifices the spatial arrangement of mRNAs within tissue.
NanoString offers two robust and widely-cited platforms for multiplexed proteomics and transcriptomics of challenging neuroscience sample types such as FFPE, cell lysates, and cerebrospinal fluid. The nCounter® Analysis System and GeoMx® Digital Spatial Profiler (DSP) can be used in tandem with minimal hands-on time for bulk and spatial profiling of RNA or protein to generate accurate, repeatable, and insightful results in less than 24 hours that get you to your next neuroscience publication faster.
Select from curated, multiplexed nCounter Gene Expression Panels and/or GeoMx DSP Protein assays and the Whole Transcriptome Atlas to build your own experiment. Take advantage of embedded CNS and immune cell typing signatures to quantify the relative abundance of 5 CNS cell types and 14 different immune cell types.
Profile 770 human or mouse genes involved in six fundamental themes of neurodegeneration. Includes CNS cell typing signatures.
Study neuroinflammatory disorders or CNS infections with assessment of 23 pathways across 770 human or mouse genes. Includes CNS and immune cell typing signatures.
Translate mouse models of Alzheimer’s disease to human studies with a panel that includes 30 clinically derived AD-associated modules discovered in the AMP-AD consortium study
Decipher the role of astrocytes, microglia, and oligodendrocytes in health and disease with a panel of 770 human or mouse genes. Includes CNS and immune cell typing signatures.
Profile 96+ human proteins associated with CNS cells, Alzheimer’s, and Parkinson’s from a single FFPE tissue section or fresh frozen tissue slice with spatial resolution. Customize your assay by adding protein targets of your choice.
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.