Abstract
Prostate cancer (PC) is one of the most common malignancies in men. The increase in the number of PC survivors is associated with many problems including cognitive impairment. Early detection of such problems facilitates timely protective intervention. This study examined the association between prostate-specific antigen (PSA) or testosterone (T) levels and cognitive function in patients undergoing radical prostatectomy. Such a correlation could help identify patient groups at risk of cognitive impairment. Participants underwent clinical (demographic data, medical history, physical examination, and blood analyses) and neuropsychological assessment (cognitive test battery). Preoperative PSA or T levels were not associated with cognitive function. However, long-term follow-up after prostatectomy showed a strong correlation between PSA levels and the results of verbal memory and executive function tests. A trend toward significance was also observed for visuospatial memory. The levels of free T and total T were not correlated with cognitive function. Only the levels of free T after hormonal treatment were significantly correlated with executive functions. Comorbid diabetes affected these correlations. In conclusion, PSA levels at a distant postoperative time and free T level after hormonal treatment may be biomarkers of cognitive function.
Highlights
Prostate cancer (PC) is one of the most common malignancies in men [1]
This study examined the potential association of biochemical parameters that are routinely measured in PC, such as prostate-specific antigen (PSA) or testosterone, with cognitive function
Comparison of the clinicopathological and demographic characteristics of the two groups (Table 2) showed that the group with PSA > 0.1 ng/mL at 6 weeks postoperatively had a lower incidence of arterial hypertension and higher rates of disease severity before surgery according to GG classification
Summary
Prostate cancer (PC) is one of the most common malignancies in men [1]. Despite considerable progress in the detection and treatment of PC, it remains the fifth leading cause of death worldwide, with approximately 375,000 deaths per year. The pathogenetic mechanisms underlying these dysfunctions remain unclear They seem to be multifactorial and related to both the cancer itself and to treatments such as radiochemotherapy, hormone therapy, and surgery [4,5,9,10]. The probable link of PC and cognitive dysfunction is supported by some biological processes including through abnormal accumulation of proteins, neuroinflammation, oxidative stress, and neuronal cell death. These changes can lead to the breakdown of the blood-brain barrier and promote key pathways for the development of cognitive disorders (such as brain insulin resistance, mitochondrial dysfunction, and deposits of neurotoxic beta-amyloid oligomers, synaptic loss, neuronal dysfunction, and cell death) [11,12,13]
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