Neuroinflammatory disorders are the chronic inflammation of the central nervous system. It may be the result of an acute event like traumatic brain injury or a viral infection. Neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease and neuropsychiatric disorders such as autism and schizophrenia have a neuroinflammatory component. A hallmark pathophysiological response of neuroinflammation is the activation of microglia which release cytokines such as IL-1 beta or IL-16 alpha. Cytokine release and up-regulation impact neurotransmitter levels such as glutamate and dopamine which in turn affect the central nervous system.
Neuroscience 2019 Scientific Posters
Discover new approaches and technologies to fuel your next neuroscience discovery. Check out our scientific posters from Neuroscience 2019.
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In Vitro Neuroinflammation Models and Services
When deciding on a neuroinflammatory assay, it's important to account for all the relevant factors that contribute to this complex system. Depending on your stage of drug development, you may want to screen a library using cell-based assays such as translocator protein (TSPO) expression, cell death, or cytokine release.
In Vitro Models
- iPSC-derived astrocytes, microglia & neurons
- Murine microglia isolation
- Human microglial cultures
- Murine cortical glial and mixed cultures
In Vitro Assays
- Cytokine release
- LPS-induced inflammation
- Nitric oxide production
- Macrophage activation
- Phagocytosis assays
Murine Primary Neuron-Glia Co-Culture Immunofluorescence with Neuronal Marker, Synapsin-1 (green) and Glial Marker, GFAP (red).
LPS-Induced Neuroinflammation - New Treatment Strategies
In Vivo Neuroinflammation Models and Services
Once you've identified your lead compound, choosing an in vivo model may be the next step. This could be a drug-induced model or a transgenic model. We can assess whether your compound reaches the brain, if it passes the blood-brain barrier, and what happens to biomarker levels from the blood or cerebrospinal fluid (CSF) samples.
In Vivo Models
In Vivo Model of Neuroinflammation
Nuclear imaging (SPECT/ PET) of an in vivo model of neuroinflammation using TSPO as a target to activated glia.
Frequently Asked Questions (FAQs) for Neuroinflammation
Why is the brain no longer considered immune-privileged?
For a long time, the blood-brain barrier (BBB) was thought to be a protector of proinflammatory responses from the periphery. However, recent data have revealed that peripheral immune cells can cross the intact BBB, and that CNS neurons and glia actively regulate macrophage and lymphocyte responses. This newer view of CNS immune privilege is opening the door for therapies designed to harness autoreactive lymphocyte responses.
Is neuroinflammation protective or toxic?
Neuroinflammation is defined as an inflammatory reaction within the central nervous system that arises as a mechanism to protect the brain and spinal cord against potential harm from a variety of toxic stimuli, such as protein aggregates, neuronal injury, and infection. Cytokine release and signaling from the peripheral side of the BBB can also trigger a mirrored response of glial activation and cytokine release on the brain side of BBB. The process of neuroimmune signaling that can trigger inflammation challenges the health of the brain, where too much is always detrimental to the health of neurons.