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Updated: May 31, 2026

Quantifying Cognitive Decrements Caused by Cranial Radiotherapy

Quantifying Cognitive Decrements Caused by Cranial Radiotherapy

Published on: October 18, 2011

Caffeine attenuates cisplatin induced microglial reactivity and cognitive dysfunction.

Alfredo Oliveros^1,2,3, Ivan Loncar¹, Marwan Mostafa¹

¹Department of Neurosurgery, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ, United States.

Frontiers in Molecular Neuroscience

|May 29, 2026

Summary

Caffeine may combat chemotherapy-induced cognitive impairments (CICI) by blocking adenosine A2A receptors (A2AR). This study shows caffeine reduces neuroinflammation and cognitive deficits in mice treated with cisplatin, offering a potential strategy for chemobrain recovery.

Keywords:

adenosine receptor 2A caffeine chemobrain chemofog cisplatin microglia neurogenesis

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Published on: October 18, 2011

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Published on: March 16, 2018

Area of Science:

Neuroscience
Oncology
Pharmacology

Background:

Chemotherapy, while extending cancer survivorship, causes neurotoxic side effects impacting cognitive function.
Chemotherapy-induced cognitive impairments (CICI), or chemobrain, are linked to neuroinflammation.
Adenosine A2A receptors (A2AR) in the hippocampus are implicated in CICI, but their role in cisplatin-induced neuroinflammation is unclear.

Purpose of the Study:

To investigate if A2A receptor signaling mediates cisplatin-induced neuroinflammation and cognitive deficits.
To determine if caffeine, an A2A receptor antagonist, can mitigate these cisplatin-induced effects.

Main Methods:

Utilized a mouse model with cisplatin-induced cognitive impairments (CICI).
Examined microglial morphology and density following cisplatin treatment.
Assessed the effects of caffeine administration on physical recovery, motor function, hippocampal neurogenesis, dendritic spine density, and memory.

Main Results:

Cisplatin induced a primed microglial phenotype, indicating neuroinflammation.
Caffeine attenuated cisplatin-induced microglial changes.
Caffeine mitigated body weight loss, accelerated physical recovery, protected against motor deficits, and preserved hippocampal structure and function.

Conclusions:

A2A receptor-mediated microglial priming is associated with chemobrain.
A2A receptor inhibition by caffeine shows potential for ameliorating physical and cognitive impairments caused by chemotherapy.