RT Journal Article
SR Electronic
T1 The protective effect of Astaxanthin on scopolamine - induced Alzheimer’s model in mice
JF Neurosciences Journal
JO Neurosciences (Riyadh)
FD Prince Sultan Military Medical City
SP 103
OP 112
DO 10.17712/nsj.2024.2.20230060
VO 29
IS 2
A1 Magadmi, Rania
A1 Nassibi, Sara
A1 Kamel, Fatemah
A1 Al-Rafiah, Aziza R.
A1 Bakhshwin, Duaa
A1 Jamal, Maha
A1 Alsieni, Mohammed
A1 Burzangi, Abdulhadi S.
A1 Zaher, M. A. F
A1 Bendary, Mohammed
YR 2024
UL http://nsj.org.sa/content/29/2/103.abstract
AB Objectives: To investigate the fundamental mechanisms of the neuroprotective impact of Astaxanthin (AST) in a mouse model of Alzheimer’s disease (AD) induced by scopolamine.Methods: This research constituted an in vivo animal study encompassing 36 adult male mice, divided into 6 groups: Control, 100 mg/kg AST, 2 mg/kg scopolamine (AD group), 100 mg/kg AST+2 mg/kg scopolamine, 3 mg/kg galantamine+2 mg/kg scopolamine, and 100 mg/kg AST+3 mg/kg galantamine+2 mg/kg scopolamine. After 14 days, the mice’s short-term memory, hippocampus tissue, oxidative and inflammatory markers were evaluated.Results: The AST demonstrated a beneficial influence on short-term memory and a reduction in acetylcholinesterase activity in the brain. It exhibited neuroprotective and anti-amyloidogenic properties, significantly decreased pro-inflammatory markers and oxidative stress, and reversed the decline of the Akt-1 and phosphorylated Akt pathway, a crucial regulator of abnormal tau. Furthermore, AST enhanced the effect of galantamine in reducing inflammation and oxidative stress.Conclusion: The findings indicate that AST may offer therapeutic benefits against cognitive dysfunction in AD. This is attributed to its ability to reduce oxidative stress, control neuroinflammation, and enhance Akt-1 and pAkt levels, thereby underscoring its potential in AD treatment strategies.