- Abstracts will be reviewed by at least two reviewers.
- Selected abstracts will be published in a supplement issue of the Neuroendocrinology.
- All abstracts will be included in the Congress Abstract Book.
- Abstracts should be submitted through the ONLINE SUBMISSION SYSTEM.
- Prepare your abstract using the abstract format (click to download the abstract template).
- Abstracts must be submitted in English
- Oral communication at the meeting can be presented in English orTurkish
- Poster communication at the meeting must be presented in English (Poster size must be 70x90cm, vertically).
- To complete the registration process, please fill in THE REGISTRATION FORM.
- It should be a maximum 300 words excluding the title, authors and affiliations
- Names should be written in full (example: Ahmet Ayar)
- Academic titles should not be indicated with author names
- Authors’ affiliations should be clearly given as in the abstract example below
- Abstracts should be structured as AIM, METHODS, RESULTS, CONCLUSION
- If there is any acknowledgement, it should be indicated at the end of the abstract
- Abstracts with insufficient information (less than 200 words) will not be accepted.
Example for Abstract Format:
Neuroprotective Efficacy of the Peroxisome Proliferator Activated Receptor Gamma Ligand in Chronic Cerebral Hypoperfusion
Hale Sayan Ozaçmak1, Figen Barut1, Ewa Jakubowska Dogru2
1) Zonguldak Karaelmas University, Medical School, Department of Physiology, Zonguldak, Turkey
2) Middle East Technical University, Department of Biology, Ankara, Turkey
AIM: Chronic cerebral hypoperfusion can cause learning and memory impairment and neuronal damage resembling the effects observed in vascular dementia. The present study was designed to investigate possible neuroprotective effects of rosiglitazone, a PPAR-gamma agonist, in rat model of chronic cerebral hypoperfusion.
METHODS: Adult male Wistar rats were used. Cerebral hypoperfusion was induced by permanent bilateral occlusion of the common carotid arteries. Oral administration of rosiglitazone (1.5, 3, and 6 mg/kg/day) or vehicle was carried out for 5 weeks, starting one week before the surgery. Cognitive performance was assessed using the Morris water maze. The density of the OX-42-labeled microglial activation and hippocampal neuronal death were estimated. Synaptogenesis was also evaluated by the measurement of synaptophysin, the pre-synaptic vesicular protein, and level via western blotting technique.
RESULTS: Cerebral hypoperfusion for 30 days induced a significant cognitive impairment along with hyperactivation of microglial and astroglial cells, hippocampal neuronal loss, and reduction of synaptophysin level. The escape latencies for both 3 and 6 mg/kg of rosiglitazone-treated groups were significantly shorter than in the ischemia control group (p<0.05). For the group treated with 3 mg/kg of rosiglitazone, the number of OX-42 positive cells significantly decreased, as compared with two other treatment groups (p<0.05). Compared to the sham-operated group, the amounts of synaptophysin protein in the ischemia, 1.5 mg/kg, and 3 mg/kg rosiglitazone-treated groups, were statistically lower (p<0.05), whereas in the group treated with 6 mg/kg of rosiglitazone, no significant difference was noted.
CONCLUSION: Our results suggest that the chronic administration of rosiglitazone significantly prevents chronic cerebral hypoperfusion-induced brain damage, at least, partly through suppressing glial activation and preserving synaptic plasticity.
Acknowledgement: This study was supported by TUBITAK (Project # 112S450).
METHODS: Adult male Wistar rats were used. Cerebral hypoperfusion was induced by permanent bilateral occlusion of the common carotid arteries. Oral administration of rosiglitazone (1.5, 3, and 6 mg/kg/day) or vehicle was carried out for 5 weeks, starting one week before the surgery. Cognitive performance was assessed using the Morris water maze. The density of the OX-42-labeled microglial activation and hippocampal neuronal death were estimated. Synaptogenesis was also evaluated by the measurement of synaptophysin, the pre-synaptic vesicular protein, and level via western blotting technique.
RESULTS: Cerebral hypoperfusion for 30 days induced a significant cognitive impairment along with hyperactivation of microglial and astroglial cells, hippocampal neuronal loss, and reduction of synaptophysin level. The escape latencies for both 3 and 6 mg/kg of rosiglitazone-treated groups were significantly shorter than in the ischemia control group (p<0.05). For the group treated with 3 mg/kg of rosiglitazone, the number of OX-42 positive cells significantly decreased, as compared with two other treatment groups (p<0.05). Compared to the sham-operated group, the amounts of synaptophysin protein in the ischemia, 1.5 mg/kg, and 3 mg/kg rosiglitazone-treated groups, were statistically lower (p<0.05), whereas in the group treated with 6 mg/kg of rosiglitazone, no significant difference was noted.
CONCLUSION: Our results suggest that the chronic administration of rosiglitazone significantly prevents chronic cerebral hypoperfusion-induced brain damage, at least, partly through suppressing glial activation and preserving synaptic plasticity.
Acknowledgement: This study was supported by TUBITAK (Project # 112S450).