scholarly journals Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimer’s Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Lulin Nie ◽  
Junxia Xia ◽  
Honglian Li ◽  
Zaijun Zhang ◽  
Ying Yang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Impairment ◽  
Potential Candidate ◽  
Ginsenoside Rg1 ◽  
Behavioral Tests ◽  
Behavioral Deficits ◽  
Behavioral Abnormalities ◽  
Candidate Drug ◽  
Proteomic Change

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, so far, there are no effective measures to prevent and cure this deadly condition. Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Proteomic results revealed a total of 28 differentially expressed hippocampal proteins between Rg1-treated and nontreated 3xTg-AD mice. Among these proteins, complexin-2 (CPLX2), synapsin-2 (SYN2), and synaptosomal-associated protein 25 (SNP25) were significantly downregulated in the hippocampus of 3xTg-AD mice compared with the WT mice, and the treatment of Rg1 modulated the expression of CPLX2 and SNP25 in the hippocampus of 3xTg-AD mice. The expression of CPLX2, SYN2, and SNP25 was further validated by Western blot analysis. Taken together, we concluded that Rg1 could be a potential candidate drug to improve the behavioral deficits in AD via modulating the expression of the proteins (i.e., CPLX2, SYN2, and SNP25).

scholarly journals Stem Cells as Potential Targets of Polyphenols in Multiple Sclerosis and Alzheimer’s Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-30 ◽  
Author(s):  
Ankit Tandon ◽  
Sangh Jyoti Singh ◽  
Rajnish Kumar Chaturvedi
Keyword(s):  
Multiple Sclerosis ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Stem Cell ◽  
Therapeutic Effects ◽  
Potential Candidate ◽  
Behavioral Deficits ◽  
Cell Therapies ◽  
Proliferation And Differentiation

Alzheimer’s disease (AD) and multiple sclerosis are major neurodegenerative diseases, which are characterized by the accumulation of abnormal pathogenic proteins due to oxidative stress, mitochondrial dysfunction, impaired autophagy, and pathogens, leading to neurodegeneration and behavioral deficits. Herein, we reviewed the utility of plant polyphenols in regulating proliferation and differentiation of stem cells for inducing brain self-repair in AD and multiple sclerosis. Firstly, we discussed the genetic, physiological, and environmental factors involved in the pathophysiology of both the disorders. Next, we reviewed various stem cell therapies available and how they have proved useful in animal models of AD and multiple sclerosis. Lastly, we discussed how polyphenols utilize the potential of stem cells, either complementing their therapeutic effects or stimulating endogenous and exogenous neurogenesis, against these diseases. We suggest that polyphenols could be a potential candidate for stem cell therapy against neurodegenerative disorders.

scholarly journals Loss of ferroportin induces memory impairment by promoting ferroptosis in Alzheimer’s disease

2021 ◽  
Author(s):  
Wen-Dai Bao ◽  
Pei Pang ◽  
Xiao-Ting Zhou ◽  
Fan Hu ◽  
Wan Xiong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Impairment ◽  
Iron Homeostasis ◽  
Critical Role ◽  
Gene Set Enrichment Analysis ◽  
Molecular Characteristics ◽  
Intracellular Iron

AbstractIron homeostasis disturbance has been implicated in Alzheimer’s disease (AD), and excess iron exacerbates oxidative damage and cognitive defects. Ferroptosis is a nonapoptotic form of cell death dependent upon intracellular iron. However, the involvement of ferroptosis in the pathogenesis of AD remains elusive. Here, we report that ferroportin1 (Fpn), the only identified mammalian nonheme iron exporter, was downregulated in the brains of APPswe/PS1dE9 mice as an Alzheimer’s mouse model and Alzheimer’s patients. Genetic deletion of Fpn in principal neurons of the neocortex and hippocampus by breeding Fpnfl/fl mice with NEX-Cre mice led to AD-like hippocampal atrophy and memory deficits. Interestingly, the canonical morphological and molecular characteristics of ferroptosis were observed in both Fpnfl/fl/NEXcre and AD mice. Gene set enrichment analysis (GSEA) of ferroptosis-related RNA-seq data showed that the differentially expressed genes were highly enriched in gene sets associated with AD. Furthermore, administration of specific inhibitors of ferroptosis effectively reduced the neuronal death and memory impairments induced by Aβ aggregation in vitro and in vivo. In addition, restoring Fpn ameliorated ferroptosis and memory impairment in APPswe/PS1dE9 mice. Our study demonstrates the critical role of Fpn and ferroptosis in the progression of AD, thus provides promising therapeutic approaches for this disease.

P1-168: Behavioral abnormalities are associated with milder dementia in Alzheimer's disease than in dementia with lewy bodies

2011 ◽  
Vol 7 ◽  
pp. S165-S166
Author(s):  
David P. Salmon ◽  
Eliezer Masliah ◽  
Douglas Galasko ◽  
Guerry Peavy ◽  
Lawrence Hansen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies ◽  
Behavioral Abnormalities

The Semantic Memory Impairment of Alzheimer's Disease: Category-Specific?

Cortex ◽  
1996 ◽  
Vol 32 (1) ◽  
pp. 143-153 ◽  
Author(s):  
Lynette J. Tippett ◽  
Murray Grossman ◽  
Martha J. Farah
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Semantic Memory ◽  
Memory Impairment ◽  
Disease Category

P4-093: Semantic memory impairment in Alzheimer's disease and frontotemporal dementia is associated with semantic network degradation

2011 ◽  
Vol 7 ◽  
pp. S734-S734
Author(s):  
Kimiko Domoto-Reilly ◽  
Daisy Sapolsky ◽  
Michael Brickhouse ◽  
Mark Hollenbeck ◽  
Brad Dickerson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Semantic Memory ◽  
Memory Impairment ◽  
Semantic Network

Effects of Gossypium herbaceam Extract Administration on the Learning and Memory Function in the Naturally Aged Rats: Neuronal Niche Improvement1

2012 ◽  
Vol 31 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Yanyong Liu ◽  
Haji Akber Aisa ◽  
Chao Ji ◽  
Nan Yang ◽  
Haibo Zhu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Neuroprotective Effect ◽  
Memory Function ◽  
Aged Rats

Aging-associated cognitive impairment is an important health care issue since individuals with mild cognitive impairment are more likely to develop Alzheimer’s disease. In the present study, the protective effect of Gossypium herbaceam extracts (GHE) on learning and memory impairment associated with aging were examined in vivo using Morris water maze and step through task. Furthermore, the antioxidant activity and neuroprotective effect of GHE was investigated with methods of histochemistry and biochemistry. These data showed that oral administration with GHE at the doses of 35, 70, and 140 mg/kg exerted an improved effect on the learning and memory impairment in aged rats. Subsequently, GHE afforded a beneficial action on eradication of free radicals without influence on the activity of glutathione peroxidase and superoxide dismutase. GHE treatment enhanced the expression levels of nerve growth factor. Meanwhile, proliferation of neural progenitor cells was elevated in hippocampus after treatment with GHE. Taken together, neurogenic niche improvement could be involved in the mechanism underlying neuroprotection of GHE against aging-associated cognitive impairment. These findings suggested that GHE might be a potential agent as cognitive-enhancing drugs that delay or halt mild cognitive impairment progression to Alzheimer’s disease or treatment of aging-associated cognitive impairment.

A multifunctional compound ebselen reverses memory impairment, apoptosis and oxidative stress in a mouse model of sporadic Alzheimer's disease

2019 ◽  
Vol 109 ◽  
pp. 107-117 ◽  
Author(s):  
Franciele Martini ◽  
Suzan Gonçalves Rosa ◽  
Isabella Pregardier Klann ◽  
Bruna Cruz Weber Fulco ◽  
Fabiano Barbosa Carvalho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Memory Impairment ◽  
Sporadic Alzheimer’S Disease ◽  
And Oxidative Stress
Sign in / Sign up

Export Citation Format

Share Document