The relationship of salusins with Parkinson's Disease, Alzheimer's Disease, and acute ischemic stroke: A preliminary study

ÇAKIR M., SAÇMACI H.

Neuroscience Letters, cilt.824, 2024 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 824
  • Basım Tarihi: 2024
  • Doi Numarası: 10.1016/j.neulet.2024.137683
  • Dergi Adı: Neuroscience Letters
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Animal Behavior Abstracts, BIOSIS, CAB Abstracts, Chemical Abstracts Core, Veterinary Science Database
  • Anahtar Kelimeler: Acute Ischemic Stroke, Alzheimer's Disease, Parkinson's Disease, Salusin-α, Salusin-β
  • Yozgat Bozok Üniversitesi Adresli: Evet

Özet

Neuroinflammation, oxidative stress, and apoptosis play important roles in the pathophysiology of Alzheimer's Disease (AD), Parkinson's Disease (PD), and Acute Ischemic Stroke (AIS). Salusin-α and salusin-β peptides, which were shown to be present in many tissues, including the central nervous system, were also shown to be associated with apoptosis, inflammation, and oxidative stress. In the present study, the relationship between Salusin-α and salusin-β peptides and AD, PD, and AIS were investigated. A total of 179 people were included in the present study, including 46 AD, 44 PD, 42 AIS, and 47 controls. Plasma Salusin-α and salusin-β levels were measured with the ELISA Method. The plasma salusin-β levels of AD, PD, and AIS patients were lower than the control group at significant levels (p < 0.05). It was also found that there were correlations between salusin-α and salusin-β levels and age, triglyceride, LDL-c, total cholesterol, and hemoglobin levels. In this study, we found that salusin- β, an endogenous neuropeptide, was associated with AD, PD and AIS. The low level of salusin-β in these diseases in which neuronal damage occurs may be related to the neuroprotective properties of this endogenous peptide. Further studies are needed to fully understand the relationship between salusin-β and the pathophysiology of these diseases.