İskemik beyin hasarı sonrası nöronal sağ kalım ve nöral onarımı düzenleyen nöroimmün mekanizmalar
10.Hücresel Sinirbilim Günleri, Kastamonu, Türkiye, 28 - 30 Nisan 2023, cilt.15, sa.1, ss.8, (Özet Bildiri)
- Yayın Türü: Bildiri / Özet Bildiri
- Cilt numarası: 15
- Basıldığı Şehir: Kastamonu
- Basıldığı Ülke: Türkiye
- Sayfa Sayıları: ss.8
- Van Yüzüncü Yıl Üniversitesi Adresli: Evet
Özet
Acute ischemic stroke; is defined by sudden cessation of focal cerebral blood flow due to thrombosis or embolism. Neurons that demand high glucose and oxygen are vulnerable to ischemia. Rapid neuronal death begins due to mitochondrial dysfunction. Disruption of the blood-brain barrier causes molecules and cells in the blood, including immune cells, to leak into the ischemic brain area. Some molecules increase microvascular permeability, causing swelling (edema) of brain tissue. Acute cerebral inflammation often worsens the functional prognosis of patients. Complex interactions between immunity and brain cells initially trigger stroke pathologies. Inflammation and swelling of brain tissue resolve about one week after the stroke. During this healing phase, resident or infiltrating immune cells switch from a pro-inflammatory role to a reparative role. These cells produce neurotrophic factors and synapse-modulating molecules around the injured brain tissue for stroke recovery. This helps to restore brain tissue in the peri-infarction area, accelerate functional recovery, and reorganize neural tissues. This reflects the close relationship between reparative immune cells and neurons near and far from the infarct area. Although recovery persists for months or even years after stroke onset, these brain-endogenous repair mechanisms usually continue to disappear slowly. The lack of therapeutic drugs to accelerate neural repair later perpetuates neurological disorders. Although post-stroke recovery continues for months or even several years after stroke onset, these brain-endogenous repair mechanisms usually continue to disappear slowly, and the remaining neurological deficits then become permanent after-effects. Functional recovery after brain injury; requires reorganization of the neural circuit, remodeling of nervous tissue, restoration of blood circulation, remyelination, axonal growth, synaptic modulation, and neurogenesis. Therefore, there is a need for new-generation therapeutics that will accelerate the resolution of acute harmful inflammation, promote beneficial neuro-immune interaction, and provide better functional recovery with restorative dynamics.