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    Acute and post-acute neuromodulation induces stroke recovery by promoting survival signaling, neurogenesis, and pyramidal tract plasticity
    (Frontiers Media Sa, 2019) Çağlayan, Ahmet Burak; Beker, Mustafa Çağlar; Çağlayan, Berrak; Yalçın, Esra; Çağlayan, Aysun; Yuluğ, Burak; Hanoğlu, Lütfü; Kutlu, Selim; Doeppner, Thorsten Roland; Hermann, Dirk Matthias; Kılıç, Ertuğrul
    Repetitive transcranial magnetic stimulation (rTMS) has gained interest as a non-invasive treatment for stroke based on the data promoting its effects on functional recovery. However, the exact action mechanisms by which the rTMS exert beneficial effects in cellular and molecular aspect are largely unknown. To elucidate the effects of high- and low-frequency rTMS in the acute-ischemic brain, we examined how rTMS influences injury development, cerebral blood flow (CBF), DNA fragmentation, neuronal survival, pro- and anti-apoptotic protein activations after 30 and 90 min of focal cerebral ischemia. In addition, inflammation, angiogenesis, growth factors and axonal outgrowth related gene expressions, were analyzed. Furthermore, we have investigated the effects of rTMS on post-acute ischemic brain, particularly on spontaneous locomotor activity, perilesional tissue remodeling, axonal sprouting of corticobulbar tracts, glial scar formation and cell proliferation, in which rTMS was applied starting 3 days after the stroke onset for 28 days. In the high-frequency rTMS received animals reduced DNA fragmentation, infarct volume and improved CBF were observed, which were associated with increased Bcl-xL activity and reduced Bax, caspase-1, and caspase-3 activations. Moreover, increased angiogenesis, growth factors; and reduced inflammation and axonal sprouting related gene expressions were observed. These results correlated with reduced microglial activation, neuronal degeneration, glial scar formation and improved functional recovery, tissue remodeling, contralesional pyramidal tract plasticity and neurogenesis in the subacute rTMS treated animals. Overall, we propose that high-frequency rTMS in stroke patients can be used to promote functional recovery by inducing the endogenous repair and recovery mechanisms of the brain.
  • Küçük Resim Yok
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    Chronic manipulation of arcuate kisspeptin neurons in a(1-42) induced mouse model of alzheimer's disease
    (Karger, 2018) Aguş, Sami; Eyüboğlu, Siğnem; Solak, Hatice; Bilgin, Volkan Adem; Yavuz, Yavuz; Akkaya, Hatice; Özge, Başer; Kutlu, Selim; Aykut Bingöl, Canan; Atasoy, Deniz; Yılmaz, Bayram
    [Abstract Not Available]
  • Küçük Resim Yok
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    Effects of chronic modulation of kiss1 neurons on catecholamine levels in experimental alzheimer disease's model
    (Wiley, 2018) Aguş, Sami; Eyüboğlu, Siğnem; Solak, Hatice; Bilgin, Volkan Adem; Yavuz, Yavuz; Akkaya, Hatice; Başer, Özge; Kutlu, Selim; Bingöl, Canan Aykut; Atasoy, Deniz; Yılmaz, Bayram
    [Abstract Not Available]
  • Küçük Resim
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    Normobaric oxygen treatment improves neuronal survival functional recovery and axonal plasticity after newborn hypoxia-ischemia
    (Elsevier, 2020) Keleştemur, Taha; Beker, Mustafa Çağlar; Çağlayan, Ahmet Burak; Çağlayan, Berrak; Altunay, Serdar; Kutlu, Selim; Kılıç, Ertuğrul
    Background: Newborn hypoxia ischemia (HI) is one of the most prevalent cases in the emergency and can result from fetal hypoxia during delivery. In HI, restricted blood supply to the fetal brain may cause epilepsy or mental disorders.Methods: In the present study, seven-day-old pups were subjected HI and treated with different normobaric oxygen (NBO) concentrations (21%, 70% or 100%). In the acute phase, we analyzed infarct area, disseminate neuronal injury and surviving neurons. In addition, we studied the regulation of PTEN and MMP-9 proteins which were suggested to be activated by HI in the ischemic tissue. Moreover, long-term effects of NBO treatments were evaluated with open field, rotarod and Barnes maze tests. We also examined axonal plasticity with EGFP-AAV injection.Results: Here, we demonstrate that hyperoxic NBO concentration causes an increase in cellular survival and a decrease in the number of apoptotic cells, meanwhile inhibiting the proteins involved in cellular death mechanisms. Moreover, we found that hyperoxia decreases anxiety, promotes motor coordination and improve spatial learning and memory. Notably that axonal sprouting was promoted by hyperoxia.Conclusion: Our data suggest that NBO is a promising approach for the treatment of newborn HI, which encourage proof-of-concept studies in newborn.
  • Küçük Resim Yok
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    The role of repetative transcranial magnetic stimulation after focal cerebral ischemia
    (Wiley, 2017) Çağlayan, Ahmet Burak; Yalçın, Esra; Altunay, Serdar; Sertel, Elif; Dilden, Aysun; Karaçay, Reyda; Beker, Mustafa Çağlar; Keleştemur, Taha; Çağlayan, Berrak; Kutlu, Selim; Kılıç, Ülkan; Kılıç, Ertuğrul
    [Abstract Not Available]
  • Küçük Resim
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    Time-of-day dependent neuronal injury after ischemic stroke: Implication of circadian clock transcriptional factor bmal1 and survival kinase akt
    (Humana Press Inc, 2018) Beker, Mustafa Çağlar; Çağlayan, Berrak; Yalçın, Esra; Çağlayan, Ahmet Burak; Türkseven, Şeyma; Gürel, Büşra; Keleştemur, Taha; Sertel, Elif; Şahin, Zafer; Kutlu, Selim; Kılıç, Ülkan; Baykal, Ahmet Tarık; Kılıç, Ertuğrul
    Occurrence of stroke cases displays a time-of-day variation in human. However, the mechanism linking circadian rhythm to the internal response mechanisms against pathophysiological events after ischemic stroke remained largely unknown. To this end, temporal changes in the susceptibility to ischemia/reperfusion (I/R) injury were investigated in mice in which the ischemic stroke induced at four different Zeitgeber time points with 6-h intervals (ZT0, ZT6, ZT12, and ZT18). Besides infarct volume and brain swelling, neuronal survival, apoptosis, ischemia, and circadian rhythm related proteins were examined using immunohistochemistry, Western blot, planar surface immune assay, and liquid chromatography-mass spectrometry tools. Here, we present evidence that midnight (ZT18; 24:00) I/R injury in mice resulted in significantly improved infarct volume, brain swelling, neurological deficit score, neuronal survival, and decreased apoptotic cell death compared with ischemia induced at other time points, which were associated with increased expressions of circadian proteins Bmal1, PerI, and Clock proteins and survival kinases AKT and Erk-1/2. Moreover, ribosomal protein S6, mTOR, and Bad were also significantly increased, while the levels of PRAS40, negative regulator of AKT and mTOR, and phosphorylated p53 were decreased at this time point compared to ZT0 (06:00). Furthermore, detailed proteomic analysis revealed significantly decreased CSKP, HBB-1/2, and HBA levels, while increased GNAZ, NEGR1, IMPCT, and PDE1B at midnight as compared with early morning. Our results indicate that nighttime I/R injury results in less severe neuronal damage, with increased neuronal survival, increased levels of survival kinases and circadian clock proteins, and also alters the circadian-related proteins.