چکیده:
Chemotherapy-related cognitive impairment (CRCI), commonly referred to as chemobrain, is among the most prevalent and disabling long-term toxicities of systemic chemotherapy, substantially impairing quality of life and functional independence in cancer survivors. Despite increasing recognition of its clinical significance, no pharmacological intervention has yet been approved for its prevention or treatment. Contemporary evidence indicates that CRCI results from the convergence of neuroinflammation, oxidative stress, mitochondrial dysfunction, impaired neurogenesis, synaptic dysfunction, and neuronal apoptosis, highlighting the need for therapeutic approaches capable of modulating multiple interconnected pathogenic pathways rather than a single molecular target [1-4]. Nevertheless, the major challenge in developing neuroprotective strategies for oncology extends beyond the complexity of CRCI itself. A persistent concern is that protecting normal neural tissue may inadvertently reduce the cytotoxic efficacy of chemotherapy. Therefore, an ideal supportive therapy should preserve cognitive function while remaining fully compatible with—and preferably enhancing—the antitumor activity of anticancer treatment.
نوع مطالعه: Letter to Editor |
موضوع مقاله:
Cellular and molecular Neuroscience
دریافت: 1405/4/17 | پذیرش: 1405/6/14
دریافت: 1405/4/17 | پذیرش: 1405/6/14
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