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Microglia in Cancer Therapy-Related Cognitive Impairment
Erin M Gibson1, Michelle Monje2
1Department of Psychiatry and Behavioral Sciences, Stanford University, Palo Alto, CA 94305, USA.
Abstract:
Millions of cancer survivors experience a persistent neurological syndrome that includes deficits in memory, attention, information processing, and mental health. Cancer therapy-related cognitive impairment can cause mild to severe disruptions to quality of life for these cancer survivors. Understanding the cellular and molecular underpinnings of this disorder will facilitate new therapeutic strategies aimed at ameliorating these long-lasting impairments. Accumulating evidence suggests that a range of cancer therapies induce persistent activation of the brain's resident immune cells, microglia. Cancer therapy-induced microglial activation disrupts numerous mechanisms of neuroplasticity, and emerging findings suggest that this impairment in plasticity is central to cancer therapy-related cognitive impairment. This review explores reactive microglial dysregulation of neural circuit structure and function following cancer therapy.
Insights
Cancer therapies can cause long-lasting cognitive impairment by activating brain immune cells called microglia. This microglial activation disrupts neuroplasticity, impacting memory and attention in cancer survivors.
Area of Science:
- Neuroscience
- Oncology
- Immunology
Background:
- Cancer survivors often face persistent neurological issues, including cognitive deficits affecting memory, attention, and processing.
- Cancer therapy-related cognitive impairment significantly impacts survivors' quality of life, necessitating research into its underlying mechanisms.
Purpose of the Study:
- To explore the cellular and molecular basis of cancer therapy-related cognitive impairment.
- To investigate the role of microglial activation in long-lasting cognitive deficits after cancer treatment.
Main Methods:
- This review synthesizes accumulating evidence on microglial activation following cancer therapy.
- It examines the disruption of neuroplasticity mechanisms by cancer therapy-induced microglial activation.
Main Results:
- Evidence suggests that various cancer therapies lead to persistent activation of microglia, the brain's immune cells.
- This microglial activation is implicated in disrupting neuroplasticity, a key factor in cognitive impairment.
Conclusions:
- Reactive microglial dysregulation of neural circuits is central to cancer therapy-related cognitive impairment.
- Understanding these mechanisms is crucial for developing therapeutic strategies to alleviate long-term cognitive deficits in cancer survivors.
