Taurine Prevents Passive Avoidance Memory Impairment, Accumulation of Amyloid-β Plaques, and Neuronal Loss in the Hippocampus of Scopolamine-Treated Rats

2019 ◽  
Vol 51 (3) ◽  
pp. 171-179 ◽  
Author(s):  
S. Gorgani ◽  
M. Jahanshahi ◽  
L. Elyasi
2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Jin Bae Weon ◽  
Min Rye Eom ◽  
Youn Sik Jung ◽  
Eun-Hye Hong ◽  
Hyun-Jeong Ko ◽  
...  

Codonopsis lanceolata(C. lanceolata) is a traditional medicinal plant used for the treatment of certain inflammatory diseases such as asthma, tonsillitis, and pharyngitis. We evaluated whether steamed and fermentedC. lanceolata(SFC) extract improves amyloid-β- (Aβ-) induced learning and memory impairment in mice. The Morris water maze and passive avoidance tests were used to evaluate the effect of SFC extract. Moreover, we investigated acetylcholinesterase (AChE) activity and brain-derived neurotrophic factor (BDNF), cyclic AMP response element-binding protein (CREB), and extracellular signal-regulated kinase (ERK) signaling in the hippocampus of mice to determine a possible mechanism for the cognitive-enhancing effect. Saponin compounds in SFC were identified by Ultra Performance Liquid Chromatography-Quadrupole-Time-of-Flight Mass Spectrometry (UPLC-Q-TOF-MS). SFC extract ameliorated amyloid-β-induced memory impairment in the Morris water maze and passive avoidance tests. SFC extract inhibited AChE activity and also significantly increased the level of CREB phosphorylation, BDNF expression, and ERK activation in hippocampal tissue of amyloid-β-treated mice. Lancemasides A, B, C, D, E, and G and foetidissimoside A compounds present in SFC were determined by UPLC-Q-TOF-MS. These results indicate that SFC extract improves Aβ-induced memory deficits and that AChE inhibition and CREB/BDNF/ERK expression is important for the effect of the SFC extract. In addition, lancemaside A specifically may be responsible for efficacious effect of SFC.


2021 ◽  
pp. 113313
Author(s):  
Mitra Khakpoor ◽  
Salar Vaseghi ◽  
Mohammad-Hossein Mohammadi-Mahdiabadi-Hasani ◽  
Mohammad Nasehi

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Andre F. Batista ◽  
Tayná Rody ◽  
Leticia Forny-Germano ◽  
Suzana Cerdeiro ◽  
Maria Bellio ◽  
...  

Abstract Background The lack of effective treatments for Alzheimer’s disease (AD) reflects an incomplete understanding of disease mechanisms. Alterations in proteins involved in mitochondrial dynamics, an essential process for mitochondrial integrity and function, have been reported in AD brains. Impaired mitochondrial dynamics causes mitochondrial dysfunction and has been associated with cognitive impairment in AD. Here, we investigated a possible link between pro-inflammatory interleukin-1 (IL-1), mitochondrial dysfunction, and cognitive impairment in AD models. Methods We exposed primary hippocampal cell cultures to amyloid-β oligomers (AβOs) and carried out AβO infusions into the lateral cerebral ventricle of cynomolgus macaques to assess the impact of AβOs on proteins that regulate mitochondrial dynamics. Where indicated, primary cultures were pre-treated with mitochondrial division inhibitor 1 (mdivi-1), or with anakinra, a recombinant interleukin-1 receptor (IL-1R) antagonist used in the treatment of rheumatoid arthritis. Cognitive impairment was investigated in C57BL/6 mice that received an intracerebroventricular (i.c.v.) infusion of AβOs in the presence or absence of mdivi-1. To assess the role of interleukin-1 beta (IL-1β) in AβO-induced alterations in mitochondrial proteins and memory impairment, interleukin receptor-1 knockout (Il1r1−/−) mice received an i.c.v. infusion of AβOs. Results We report that anakinra prevented AβO-induced alteration in mitochondrial dynamics proteins in primary hippocampal cultures. Altered levels of proteins involved in mitochondrial fusion and fission were observed in the brains of cynomolgus macaques that received i.c.v. infusions of AβOs. The mitochondrial fission inhibitor, mdivi-1, alleviated synapse loss and cognitive impairment induced by AβOs in mice. In addition, AβOs failed to cause alterations in expression of mitochondrial dynamics proteins or memory impairment in Il1r1−/− mice. Conclusion These findings indicate that IL-1β mediates the impact of AβOs on proteins involved in mitochondrial dynamics and that strategies aimed to prevent pathological alterations in those proteins may counteract synapse loss and cognitive impairment in AD.


2020 ◽  
Vol 74 (1) ◽  
pp. 245-259
Author(s):  
Mona Abdelhamid ◽  
Cha-Gyun Jung ◽  
Chunyu Zhou ◽  
Mohammad Abdullah ◽  
Manabu Nakano ◽  
...  
Keyword(s):  

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Hyeon Yong Lee ◽  
Jin Bae Weon ◽  
Youn Sik Jung ◽  
Nam Young Kim ◽  
Myong Ki Kim ◽  
...  

Aronia melanocarpa(A. melanocarpa)berriesare a fruit with a marked antioxidant effect. The objective of this study was to confirm the effect ofA. melanocarpa berriesextract against scopolamine-induced memory impairment in mice using the Morris water maze and passive avoidance test. Moreover, we determined a possible mechanism of the cognitive-enhancing effect involving AChE activity and BDNF and p-CREB expression in the hippocampus of mice.A. melanocarpa berriesextract attenuated the learning and memory impairment induced by scopolamine in the Morris water maze (79.3 ± 0.8 s of 200 mg/kg and 64.4 ± 10.7 s of 400 mg/kg on day 4) and passive avoidance tests (46.0 ± 41.1 s of 200 mg/kg and 25.6 ± 18.7 s of 400 mg/kg).A. melanocarpa berriesextract reduced the acetylcholinesterase level in the hippocampus of scopolamine-injected mice and increased BDNF and p-CREB expression in the hippocampus. The major compound, cyanidin-3-O-galactoside, also reversed memory impairment. These results showed thatA. melanocarpa berriesextract improved memory impairment by inhibiting AChE and increasing BDNF and p-CREB expression, and cyanidin-3-O-galactoside may be responsible for the effect ofA. melanocarpa berriesextract.


2019 ◽  
Author(s):  
Maryam Sarbishegi ◽  
Hamidreza Mahmoudzadeh-sagheb ◽  
Zahra Heidari ◽  
Farzaneh Baharvand

Abstract- Several studies point to an important role of neuroinflammation in Parkinson's disease (PD). Cognitive and memory impairments have been known in the early stages of PD. In the present study, we examined the effects of celecoxib (CLX), a selective inhibitor of cyclooxygenase-2 (COX-2), on hippocampus cell loss, passive avoidance memory and antioxidant status in a rat model of PD. We used the subcutaneous injection of 2.5 mg/kg/48h rotenone (ROT) for 4 weeks for induction of PD in a male Wistar rat. Animals were randomized to 4 groups (n=12): Control, sham, PD and PD+CLX group that receive celecoxib (20 mg/kg/day) for 4 weeks. Passive avoidance memory evaluated. We also determined the protective effect of CLX on a number of CA1 neurons in Nissl and TUNEL staining. Total antioxidant capacity (TAC) and malondialdehyde (MDA) a marker of lipid peroxidation in hippocampus assessed. Our findings indicated administration of CLX increase the passive avoidance memory (P<0.05), and by a decrease in apoptosis caused an increase in viable pyramidal neurons in CA1 hippocampus (P<0.01). On the other hand, CLX markedly reduced MDA level and increased TAC in the hippocampus of the PD model animal (P<0.05). It seems CLX with anti-inflammatory and antiapoptotic effect could prevent neurons loss and memory impairment which induced in PD.


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