Comment on: Reduced plasma levels of NGF and BDNF in patients with acute coronary syndromes

Abstract

We appreciate the comment by Mackin and Gallagher relative to our article about reduced plasma levels of NGF and BDNF in patients with acute coronary syndromes (ACS) [2]. Mackin and Gallagher suggested that the results may be explained by the stress. Indeed, ACS is a highly dynamic phenomenon associated with neuroendocrine and proinflammatory activation ([3], also see Mackin and Gallagher’s refs. [3,4]), and, note, including adrenal insufficiency [4]. We may argue that reduced NGF/BDNF plasma levels in ACS are not due to stress-induced elevated cortisol presence in ACS. Our previous results demonstrated that various stressful events upregulated NGF ([5], reviewed in [6]). These data also revealed that the increased NGF level preceded the increased plasma cortisol and adrenocorticotropic hormone levels. Further, stress-induced increase in hypothalamic BDNF expression [7], as well as the increase in hippocampal BDNF presence in response to chronic cortisol exposure [8], were recently reported. This appears not to be consistent with the downregulation of NGF and BDNF as pointed by Mackin and Gallagher. On that background, why ‘‘cardiovascular’’ stressors such as ACS [2], (our present study), heart failure ([2], their ref. [9]), and metabolic syndrome ([2], their refs. [6,8]) are featured by decreased plasma and tissue levels of these neurotrophins is at present unclear. We wonder whether a link between testosterone [9], neurotrophin deficiency and the development of atherosclerotic cardiovascular disease could exist. From pioneering studies of Rita Levi-Montalcini it is known that there is a positive correlation between NGF and testosterone levels [10].