Ginger fermented with Schizosaccharomyces pombe alleviates memory impairment via protecting hippocampal neuronal cells in amyloid beta1–42 plaque injected mice

2018 ◽  
Vol 9 (1) ◽  
pp. 171-178 ◽  
Author(s):  
Eugene Huh ◽  
Soonmin Lim ◽  
Hyo Geun Kim ◽  
Sang Keun Ha ◽  
Ho-Young Park ◽  
...  

Ginger fermented with S. pombe alleviates AD-like memory dysfunction and neuronal degradation in an animal model.

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Hyeon Joo Ham ◽  
Yong Sun Lee ◽  
Jaesuk Yun ◽  
Dong Ju Son ◽  
Hee Pom Lee ◽  
...  

Abstract Background Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders characterized by gradual memory loss and neuropsychiatric symptoms. We have previously demonstrated that the 2-({3-[2-(1-cyclohexene-1-yl)ethyl]-6,7-dimethoxy-4-oxo-3,4-dihydro-2-quinazolinyl}sulfanyl)-N-(4-ethylphenyl)butanamide (K284-6111), the inhibitor of CHI3L1, has the inhibitory effect on memory impairment in Αβ infusion mouse model and on LPS-induced neuroinflammation in the murine BV-2 microglia and primary cultured astrocyte. Methods In the present study, we investigated the inhibitory effect of K284-6111 on memory dysfunction and neuroinflammation in Tg2576 transgenic mice, and a more detailed correlation of CHI3L1 and AD. To investigate the effects of K284-6111 on memory dysfunction, we administered K284-6111 (3 mg/kg, p.o.) daily for 4 weeks to Tg2576 mice, followed by behavioral tests of water maze test, probe test, and passive avoidance test. Results Administration of K284-6111 alleviated memory impairment in Tg2576 mice and had the effect of reducing the accumulation of Aβ and neuroinflammatory responses in the mouse brain. K284-6111 treatment also selectively inactivated ERK and NF-κB pathways, which were activated when CHI3L1 was overexpressed, in the mouse brain and in BV-2 cells. Web-based gene network analysis and our results of gene expression level in BV-2 cells showed that CHI3L1 is closely correlated with PTX3. Our result revealed that knockdown of PTX3 has an inhibitory effect on the production of inflammatory proteins and cytokines, and on the phosphorylation of ERK and IκBα. Conclusion These results suggest that K284-6111 could improve memory dysfunction by alleviating neuroinflammation through inhibiting CHI3L1 enhancing ERK-dependent PTX3 pathway.


2005 ◽  
Vol 119 (5) ◽  
pp. 1389-1395 ◽  
Author(s):  
Gordon Winocur ◽  
Carol E. Greenwood ◽  
Gerardo G. Piroli ◽  
Claudia A. Grillo ◽  
Leah R. Reznikov ◽  
...  

2015 ◽  
Vol 8 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Nattaporn Phunchago ◽  
Jintanaporn Wattanathorn ◽  
Kowit Chaisiwamongkol ◽  
Supaporn Muchimapura ◽  
Wipawee Thukham-mee

1995 ◽  
Vol 8 (2) ◽  
pp. 59-74 ◽  
Author(s):  
A. I. Tröster ◽  
J. A. Fields

Memory dysfunction is a frequent concomitant of Parkinson's disease (PD). Historically, two classes of hypotheses, focusing on different cognitive mechanisms, have been advanced to explain this memory impairment: one postulating retrieval deficits (common to several neurodegenerative disorders involving the basal ganglia), and the other postulating frontally mediated executive deficits as fundamental to memory impairment. After outlining empirical support for the retrieval deficit hypothesis, research on the more recent “frontal executive deficit hypothesis” is reviewed, and major challenges to this hypothesis are identified. It is concluded that the frontal executive deficit hypothesis cannot adequately account for all memory impairments in PD, and that a more parsimonious theoretical account might invoke a distinction between prospective and declarative memory impairments. It is suggested that there may be three subgroups of PD patients: one demonstrating prospective memory dysfunction only, one with declarative memory dysfunction only, and one with both prospective and declarative memory dysfunction. Consequently, PD might provide a useful model within which to investigate the relationship between prospective and declarative memory.


1985 ◽  
Vol 39 ◽  
pp. 175
Author(s):  
Yoshihiro Kiyota ◽  
Kazuhiro Hamajo ◽  
Masaomi Miyamoto ◽  
Akinobu Nagaoka ◽  
Yuji Nagawa

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Supaporn Muchimapura ◽  
Wipawee Thukham-Mee ◽  
Kornkanok Ingkaninan ◽  
Sakchai Wittaya-Areekul

To date, the effective preventive paradigm against mild cognitive impairment (MCI) is required. Therefore, we aimed to determine whetherMangifera indicafruit extract, a substance possessing antioxidant and cognitive enhancing effects, could improve memory impairment, cholinergic dysfunction, and oxidative stress damage in animal model of mild cognitive impairment. Male Wistar rats, weighing 180–200 g, were orally given the extract at doses of 12.5, 50, and 200 mg·kg−1BW for 2 weeks before and 1 week after the bilateral injection of AF64A (icv). At the end of study, spatial memory, cholinergic neurons density, MDA level, and the activities of SOD, CAT, and GSH-Px enzymes in hippocampus were determined. The results showed that all doses of extract could improve memory together with the decreased MDA level and the increased SOD and GSH-Px enzymes activities. The increased cholinergic neurons density in CA1 and CA3 of hippocampus was also observed in rats treated with the extract at doses of 50 and 200 mg·kg−1BW. Therefore, our results suggested thatM. indica, the potential protective agent against MCI, increased cholinergic function and the decreased oxidative stress which in turn enhanced memory. However, further researches are essential to elucidate the possible active ingredients and detail mechanism.


2019 ◽  
Vol 30 ◽  
pp. 201-207 ◽  
Author(s):  
Karem H. Alzoubi ◽  
Alaa Shatnawi ◽  
Mohammad A. Al-Qudah ◽  
Mahmoud A. Alfaqih

2007 ◽  
Vol 35 (9) ◽  
pp. 2186-2190 ◽  
Author(s):  
Tatiana Barichello ◽  
Roberta Albino Machado ◽  
Larissa Constantino ◽  
Samira S. Valvassori ◽  
Gislaine Z. Réus ◽  
...  

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