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Neurodegenerative diseases and neuroinflammation: Getting the balance right

Credit: Kateryna Kon/Shutterstock

The lack of effective treatments for neurodegenerative conditions and their associated burden on healthcare systems underscores the urgent need to identify new drug targets.

Chronic neuroinflammation, a feature common to neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and Amyotrophic Lateral Sclerosis, might be responsive to therapeutic intervention. Recent research has identified glial cells as mediators of neurodegeneration, driving disease onset and progression.

PerkinElmer | Cisbio’s Neuroscience: Neurodegenerative diseases and neuroinflammation pathways booklet collates information on the pathogenesis of the most common neurodegenerative diseases and highlights the contribution of three types of glia cells: microglia, astrocytes and oligodendrocytes, to disease.

Microglia, often referred to as the nervous system’s immune cells, monitor neuronal health. They are activated by neuronal injury or infection to produce pro-inflammatory factors (M1 phenotype) or anti-inflammatory factors (M2 phenotype). Maintaining the right balance of anti-inflammatory mediators, which allow tissue repair and healing, and pro-inflammatory mediators, to clear cellular debris and aggregated misfolded proteins, is essential to maintain a healthy brain. The activation of microglia in both Parkinson’s disease and Alzheimer’s disease seems to be tilted towards the M1 phenotype, leading to an exacerbation of inflammation and an acceleration of disease progression.

Deactivating M1 microglia, or inducing a more beneficial M2 phenotype, could lead to new therapies for neurodegeneration. In particular, modulating signaling through the receptor TREM-2 (also known as Triggering Receptor Expressed on Myeloid Cells 2) in microglia, and inhibiting the inflammasome-mediating complex containing the protein NLRP3 in these cells, are emerging as promising approaches for dampening inflammation in neurodegeneration.

A new illustrated booklet from Cisbio called Neuroscience: Neurodegenerative diseases and neuroinflammation pathways.

Astrocytes, the most abundant type of glial cells in the brain, regulate the maturation and maintenance of neuronal function. They are highly sensitive to their environment and respond quickly to injury. Like microglia, they exist in various states of activation. In some cases, they can be neuroprotective, by reducing inflammation and stimulating repair, but in others, they are neurotoxic, promoting inflammation and contributing to neuronal cell death. Activated astrocytes that release pro-inflammatory factors have been reported in Alzheimer’s disease, Parkinson’s disease and Amyotrophic Lateral Sclerosis. These cells have also been implicated in blood brain barrier breakdown, which worsens inflammation by allowing immune cell infiltration, and can increase neuronal cell death due to excessive stimulation by glutamate as their uptake of this neurotransmitter is impaired.

Oligodendrocytes are the glial cells that form myelin sheaths around nerve fibers, which allow rapid and efficient transmission of electrical impulses. There is growing evidence that oligodendrocyte dysfunction contributes to neurodegeneration, not only in diseases such as multiple sclerosis, in which the immune system attacks oligodendrocytes and damages the myelin sheath, but also in Alzheimer’s disease where reduced levels of myelin proteins have been found in the brain tissue of people with the disease.

Although great strides have been made toward understanding how the interactions between neurons and glia are disrupted in neurodegenerative disease, many aspects of inflammation-driven neurodegeneration remain unclear. Strategies to detect and modulate the activity of microglia, astrocytes and oligodendrocytes could help tilt the inflammatory balance in the right direction to treat neurodegenerative diseases more effectively.

For more information, download PerkinElmer | Cisbio’s Neuroscience: Neurodegenerative diseases and neuroinflammation pathways booklet here.


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