Neuroprotektivni potencijal moždanog neurotrofnog čimbenika u modelu Alzheimerove bolesti in vitro
| Autor: | Štulić, Katarina |
|---|---|
| Přispěvatelé: | Nedić Erjavec, Gordana, Erhardt, Julija |
| Jazyk: | chorvatština |
| Rok vydání: | 2022 |
| Předmět: |
demencija
moždani neurotrofni čimbenik oligomeri beta amiloida primarna kultura kortikalnih neurona miša vijabilnost cistotoksičnost kaspazna aktivnost PRIRODNE ZNANOSTI. Biologija viability amyloid beta oligomers primary culture of mouse cortical neurons brain derived neurotrophic factor caspase activity cytotoxicity NATURAL SCIENCES. Biology dementia |
| Popis: | Alzheimerova bolest (AB) je neurodegenerativna bolest koju karakterizira izvanstanično nakupljanje amiloidnih plakova i unutarstanično nakupljanje neurofibrilarnih snopića. Moždani neurotrofni čimbenik (BDNF) je najrašireniji neurotrofni čimbenik rasta u središnjem živčanom sustavu. Eksprimira se u hipokampusu, korteksu i bazalnom prednjem mozgu, područjima koja su vitalna za učenje, pamćenje i izvršnu funkciju. Primarna uloga BDNF-a u mozgu je promicanje preživljavanja postmitotskih neurona te rast i diferencijacija novih neurona i sinapsi. Dosadašnja istraživanja ukazuju na ulogu smanjene razine BDNF-a u AB-u gdje su gubitak sinapsi i neurona te oslabljeno pamćenje bitan dio patologije. Beta amiloid (Aβ) utječe na razine BDNF-a direktno, inhibicijom proteolitičke konverzije prekursora u konačnu formu te indirektno – interferencijom s aksonalnim transportom. S obzirom na zaštitne učinke BDNF-a na neurotoksičnost izazvanu Aβ u uvjetima in vitro i in vivo, primjena BDNF-a predstavlja potencijalnu strategiju liječenja AB-a. Cilj ovog rada je ispitati potencijalni učinak BDNF-a u prevenciji stanične smrti, odnosno promicanju preživljenja neurona, primjenom primarne kulture mišjih neurona tretiranih oligomerima Aβ kao in vitro modelom AB-a. Rezultati istraživanja potvrđuju neuroprotektivno djelovanje BDNF-a te upućuju na to da njegova primjena smanjuje apoptotsku aktivnost u modelu AB-a in vitro. Alzheimer's disease (AD) is a neurodegenerative disease characterized by extracellular accumulation of amyloid plaques and intracellular accumulation of neurofibrillary tangles. Brain derived neurotrophic factor (BDNF) is the most abundant neurotrophic growth factor in the central nervous system. It is expressed in the hippocampus, cortex and basal forebrain, areas vital for learning, memory and executive function. The primary role of BDNF in the brain is to promote the survival of postmitotic neurons and the growth and differentiation of new neurons and synapses. Previous studies suggest the role of decreased BDNF levels in AD, where synapse and neuron loss and impaired memory are an essential part of the pathology. Amyloid beta (Aβ) affects BDNF levels directly, by inhibiting the proteolytic conversion of precursors to the final form, and indirectly by interfering with axonal transport. Given the protective effects of BDNF on neuronal toxicity induced by Aβ in vitro and in vivo, the use of BDNF represents a potential strategy for the treatment of AD. The aim of this study was to examine the potential effect of BDNF in the prevention of cell death, i.e. promoting the survival of neurons, using a primary culture of mouse cortical neurons treated with Aβ oligomers as an in vitro model of AD. The results of the study confirm the neuroprotective effect of BDNF and suggest that its use reduces apoptotic activity in an in vitro model of AD. |
| Databáze: | OpenAIRE |
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