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Phosphodiesterase-5 inhibition with tadalafil exerts anti-inflammatory effects and ameliorates cognitive function and MMN parameters. Tadalafil could be a promising candidate for chronic treatment in other inflammatory pathologies associated with mild cognitive impairment.
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Read More »By using an approach combining neuropsychological tests, electrophysiological measures, and biochemical analysis, we show that tadalafil improves the psychometric and attention tests in patients with BPH/LUTS-ED, and that parameters of the “mismatch negativity” event-related brain potential were also normalized after tadalafil treatment. Moreover, tadalafil reduces the peripheral pro-inflammatory interleukins and normalize the subset of autoreactive T cells in patients with BPH/LUTS-ED. Patients with BPH/LUTS-ED in this study showed some alterations in mental processing speed and attention compared to controls, and after tadalafil treatment the scores in psychometric tests improved. MMN area improved in parallel with performance in mental processing speed and attention, as measured by DST test, given the good correlation found (r = 0.665; p = 0.018). To the best of our knowledge this is the first study on effects of tadalafil on event-related brain potentials. MMN is an auditory event-related cognitive potential that reflects an attentional trigger. Multiple neuronal elements generate the MMN wave. MMN latency depends on the response speed of the neurons, whereas the amplitude is related to the maximum response of the sum of all the neurons that respond synchronously. The area is related to the accumulated response of all neurons during the entire MMN wave until returning to basal levels. In patients with BPH/LUTS-ED there are no alterations in latency, but the amplitude and the area are reduced, which is indicative of the activation of a lower number of neurons and during shorter periods. Tadalafil treatment normalizes these parameters, indicating an improvement of cortical activity. This study agrees with those from Shim et al.14, who showed that a daily dosing with udenafil for 2 months improved cognitive function, in addition to erectile function, in patients with ED. Tadalafil has been reported to improve cognitive function in a mouse model of Alzheimer’s disease17. A study assessing the central side-effects of sildenafil on attention and memory functions in healthy young men18 reported higher amplitude of P3 component of event-related potential (ERP) suggesting a more availability of processing resources in the sildenafil condition, and an increased capacity to focus attention on streams of auditory stimuli. Our results indicate that tadalafil would exert similar effects in patients with BPH/LUTS-ED. The mechanisms by which tadalafil improves cognition in patients with BPH/LUTS-ED could be related with the function of tadalafil as PDE5 inhibitor. PDE5 is specific for cGMP hydrolysis, and enhances cGMP signaling via reducing the degradation of this cyclic nucleotide19. Patients in this study were treated with a daily low-dose of tadalafil (5 mg/day), which did not increase the amount of plasma cGMP, but had positive effects on cognitive functions in patients, given the improvement in psychometric tests and MMN parameters. As tadalafil has been reported to cross the blood-brain barrier17, it may affect attention-related processes by promoting increases of cGMP in cortical neurons. Compounds that restore pathway function and cGMP levels restore learning capacity in rats7. BPH is associated with inflammation8,9 and with chronic activation of prostate-infiltrating lymphocytes20. In this study we show that patients with BPH/LUTS-ED present higher levels of pro-inflammatory interleukins in peripheral blood. Moreover, a subset of autoreactive T lymphocytes (CD4+ CD28−) are increased in blood from these patients (about two-fold compared to controls), indicating a pro-inflammatory environment in their blood which would be affecting in some degree to cognitive functions such as attention. CD4+ CD28− T cells expand in several diseases associated with chronic inflammation (e.g. autoimmunity, atherosclerosis, etc)16.The increased amount of CD4+ CD28− T cells in patients with BPH/LUTS-ED, which can secrete inflammatory cytokines such as interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α), could be promoting the differentiation of CD4+ T cells to IL-17 producers, process in which TGF-β and IL-6 are involved, and that is amplified by TNF-α and IL-1β21. Moreover, dysregulation of the immune response in patients with BPH/LUTS-ED can be through the high expression of IL-17 that stimulates the production of IL-6, which contributes to stromal growth in BPH9. In our study, patients with BPH/LUTS-ED showed increased levels of pro-inflammatory cytokines IL-6, and IL-17. IL-17 is an important player in the establishment of prostatic inflammation, and can be considered a modulator of BPH immune responses, by maintaining the local inflammatory microenvironment and amplifying the damage to prostatic tissue8.
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Read More »In patients with BPH/LUTS-ED, PDE5 inhibition by tadalafil treatment exerts an anti-inflammatory effect by normalizing the levels of these proinflammatory interleukins and the levels of autoreactive T lymphocytes. This result agrees with Vignozzi et al.22, who demonstrated that tadalafil possesses antioxidant as well as antinflammatory action in addition to its vasodilatory property, and that PDE5 inhibitors suppressed other TNFα-induced genes related to inflammation (IL-6, MCP1, IL-12, COX2). The changes observed in peripheral blood could reflect those in prostatic tissue. Moreover, this anti-inflammatory effect of tadalafil is associated to an improvement in attention and coordination functions, given the correlations found between the psychometric tests and proinflammatory interleukins, and with levels of autoreactive T-cells, as well as with IPSS scores. We also found higher serum IL-18 levels in patients with BPH/LUTS-ED than controls. This interleukin was found to be expressed at significantly higher levels in BPH tissues, both rat and human, than in normal prostate tissues, and may act directly in BPH pathogenesis by inducing Thrombospondin-1 production in prostatic smooth muscle cells via Akt phosphorylation23.
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