Assessment of the neuroprotective potential of d-cycloserine and l-serine in aluminum chloride-induced experimental models of Alzheimer's disease: In vivo and in vitro studies

Creative Commons License

Tozlu O. O., TÜRKEZ H., OKKAY U., CEYLAN O., Bayram C., HACIMÜFTÜOĞLU A., ...Daha Fazla

FRONTIERS IN NUTRITION, cilt.9, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 9
  • Basım Tarihi: 2022
  • Doi Numarası: 10.3389/fnut.2022.981889
  • Dergi Adı: FRONTIERS IN NUTRITION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Directory of Open Access Journals
  • Anahtar Kelimeler: Alzheimer's disease, aluminum, D-cycloserine, L-serine, neuroprotective, neuro-nutrient, OXIDATIVE STRESS, WATER-MAZE, RAT, NEUROBLASTOMA, HIPPOCAMPUS, AGGREGATION, NEUTROPHILS, EXPRESSION, BASOPHILS, PATHOLOGY
  • Atatürk Üniversitesi Adresli: Evet

Özet

Alzheimer's disease (AD) is a neurodegenerative disease characterized by the accumulation of amyloid-beta (A beta) plaques and neurofibrillary tangles in the brain accompanied by synaptic dysfunction and neurodegeneration. No effective treatment has been found to slow the progression of the disease. Therapeutic studies using experimental animal models have therefore become very important. Therefore, this study aimed to investigate the possible neuroprotective effect of D-cycloserine and L-serine against aluminum chloride (AlCl3)-induced AD in rats. Administration of AlCl3 for 28 days caused oxidative stress and neurodegeneration compared to the control group. In addition, we found that aluminum decreases alpha -secretase activity while increasing beta -secretase and gamma -secretase activities by molecular genetic analysis. D-cycloserine and L-serine application resulted in an improvement in neurodegeneration and oxidative damage caused by aluminum toxicity. It is believed that the results of this study will contribute to the synthesis of new compounds with improved potential against AlCl3-induced neurodegeneration, cognitive impairment, and drug development research.