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Tumor Discovery The mechanism of cancer-related cognitive decline

Figure 1. Candidate mechanisms and their interrelations between cancer and cognitive impairment.

transduction pathways that regulate cell survival and death. with at least one ApoE ε4 allele had significantly lower
A common tumor suppressor gene, p53, whose mutation scores in all cognitive domains than cancer survivors who
or dysfunction can damage the cellular genome, plays an did not have ApoE ε4 allele . Furthermore, the anti-
[87]
important role in the development and progression of inflammatory property of ApoE and its involvement in
cancer. Systematic reviews have hypothesized that in aging proper neurogenesis can be affected by oxidative stress and
neurons, dysfunction of proteins that regulate the cell cycle inflammatory response induced by chemotherapy drugs .
[88]
and apoptosis, such as p53, may affect the neuronal plasticity Thus, CRCI has a complex pathogenetic mechanism in
and function, revealing a bridging role of p53 gene in the which the immune system, genetic factors, host behavior,
progression of cancer and neurodegeneration [83,84] . There and psychosocial state interact with each other as reciprocal
is evidence that DNA methylation and histone acetylation causation (Figure 1). Further clinical studies and animal
play important roles in the activation and suppression models are warranted to fully elucidate its pathogenesis.
of cancer genes, and abnormalities of these epigenetic
modifications are associated with the progression of 5. Conclusion
neurodegeneration . Apolipoprotein E (ApoE) plays a
[85]
role in neuronal repair and plasticity after injury, and its Cognitive impairment in cancer patients is more common
ε4 allele (ApoE ε4) is closely associated with AD-related than that recognized previously. CRCI may occur
cognitive impairment and craniocerebral trauma . It was before, during, or even more than 10 years after cancer
[86]
found that the cancer patients undergoing chemotherapy treatment, primarily involving four cognitive domains,

Volume 1 Issue 1 (2022) 6 https://doi.org/10.36922/td.v1i1.46