Introduction Acromegaly is a chronic disease of increased growth hormone (GH) secretion and elevated insulin-like growth factor-I (IGF-I) levels induced by a pituitary adenoma. HMGA2 (high mobility group A2) and AIP (aryl hydrocarbon receptor-interacting protein) expression levels are related to GH-secreting adenomas, and also a response to Somatostatin Analogs (SSAs). We studied SNPs in miR-107 and miR-23b that related with AIP and HMGA2 genes respectively and control their expression, and also SNP in the 3'UTR of HMGA2 gene. Our aim was to investigate genotype distributions of the studied SNPs, as well as the possible relationship between disease and/or response to SSAs treatment in patients with acromegaly. Material and Methods Genotypes were determined by qRT-PCR method from DNA materials obtained blood samples of acromegaly patients (141) and healthy individuals (99). The genotype distributions of patients and healthy groups, as well as the relationship between the clinical data of the disease and genotypes were statistically compared. Results In acromegaly patients with T-allele, p53 expression (p=0.049) was significantly higher. In patients with CT+TT genotype and T-allele who were responder to SSA-treatment Ki-67 index (respectively p=0.019, p=0.020 respectively) was higher. We did not observe the genotypes for miR-23b and miR-107 polymorphisms in the patients and control group of Turkish population. Conclusion The genetic variations of the miRNAs genes related with HMGA2 and AIP genes were not seen in our study. Although there is no relationship between HMGA2-rs1351394 polymorphism and acromegaly disease, T allele was associated with some clinical features related to adenoma in patients with acromegaly.

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Intracellular aggregation of abnormally phosphorylated tau in neurofibrillary tangles (NFTs) is a major neuropathological hallmark of Tauopathies such as Alzheimer's disease. Tau phosphorylation is controlled by the homeostasis of glycogen synthase kinase‐3β (GSK‐3β) and protein phosphatase‐2A (PP2A). Okadaic acid (OKA) is a potent inhibitor of PP2A, leading to abnormal tau phosphorylation. Brain‐derived neurotrophic factor (BDNF) is a member of the neurotrophin family and is selectively downregulated in AD brain. In this study, we investigated the effects of tau phosphorylation on secreted and cellular BDNF levels in primary cortical neurons. Primary cortical neurons were prepared from embryonic day 16 (E16) Sprague‐Dawley rat embryos. After 7 days in vitro, neurons were treated with 25 nM OKA for inducing tau hyperphosphorylation. Tau phosphorylation was assessed by Western blot using antibody against phospho‐Thr231 and non‐phosphorylated tau protein was detected with the Tau‐1 antibody. Levels of BDNF secreted to the culture medium were determined by ELISA at the 4th, 8th and 24th hours of treatment. Cellular localization and the protein expression of BNDF were determined by immunofluorescent labeling and fluorescent intensity measurements. Our results show that after 8 hours of OKA treatment, tau phosphorylation at Thr231 increased, whereas Tau‐1 signal decreased (p<0.0001) Compared with the control groups, BDNF levels in the OKA treated group were significantly lower after 4 and 24 hours of treatment (p<0.0001) but were not significantly different at 8 hours of treatment (p>0.05). While prominent BDNF immunoreactivity was seen in cytoplasm and neurites of the neurons in control groups, BDNF immunoreactivity significantly decreased in the OKA treated group (p<0.0001) and this attenuation was significant especially at neurites. Our results suggested that decreased BDNF protein levels might depend on the defects in axonal transport as a result of disrupted microtubule structure caused by tau hyperphosphorylation.