In Vitro Neuroinflammation Models and Services

When deciding on a neuroinflammatory assay, it's important to consider 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.

A murine primary in vitro model of neuroinflammation: Immunofluorescence of a neuron-glia co-culture stained with neuronal marker synapsin-1 (green) and a glial marker glial fibrillary acidic protein (GFAP; red).

In Vitro Models & Assays

 

In Vivo Neuroinflammation Models & 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, passes the blood-brain barrier, and what happens to biomarker levels from the blood or cerebrospinal fluid (CSF) samples.

Nuclear Imaging (SPECT/ PET) of an in vivo model of neuroinflammation using TSPO as a target to image activated glia.

In Vivo Models, Biomarkers & Tools

 

Neuroinflammatory Disorders

Neuroinflammatory disorders are the result of chronic inflammation in the central nervous system. It may be the result of an acute event like traumatic brain injury, a viral infection or a chronic event such as neurodegenerative disorders like Alzheimer's disease, Parkinson's disease and Huntington's disease. More recently, it’s been implicated in neuropsychiatric disorders such as autism and schizophrenia. A pathophysiological hallmark of neuroinflammation is the activation of microglia which release various cytokines and up-regulate some neurotransmitters which may in turn have deleterious effects on the central nervous system.

Charles River Presents: Neuroinflammation Video Series
 

A computer graphic image of microglia cells which are the primary immune cell of the brain and implicated in neuroinflammation.

Watch how experts in the field discuss how the gut-microbiome contributes if not precedes neurodegeneration.
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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.

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