en Cellular and molecular Neuroscience Cellular and molecular Neuroscience Letter to Editor Letter to Editor <div style="text-align: justify;"><span style="font-size:12pt"><span style="line-height:115%"><span style="font-family:Calibri,sans-serif"><span style="font-family:&quot;Times New Roman&quot;,serif">Chemotherapy-related cognitive impairment (CRCI), commonly referred to as <i>chemobrain</i>, 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&mdash;and preferably enhancing&mdash;the antitumor activity of anticancer treatment.</span></span></span></span></div> Chemotherapy-related cognitive impairment -Chemobrain -Acetyl-11-keto-β-boswellic acid (AKBA) -Drug repurposing -Neuroprotection -Supportive oncology 0 0 http://bcn.iums.ac.ir/browse.php?a_code=A-10-8660-1&slc_lang=en&sid=1 Zahra Nazari Taloki zahra_nazari_taloki@yahoo.com 13700319475328460059201 13700319475328460059201 Yes Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.