scholarly journals Front Cover: Ameliorating Activity of Ishige okamurae on the Amyloid Beta–Induced Cognitive Deficits and Neurotoxicity through Regulating ERK, p38 MAPK, and JNK Signaling in Alzheimer's Disease–Like Mice Model

2020 ◽  
Vol 64 (12) ◽  
pp. 2070028
Author(s):  
Oh Yun Kwon ◽  
Seung Ho Lee
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
P38 Mapk ◽  
Amyloid Beta ◽  
Cognitive Deficits ◽  
Mice Model ◽  
Front Cover ◽  
Jnk Signaling ◽  
Ishige Okamurae

GINKGETIN AMELIORATES NEUROPATHOLOGICAL CHANGES IN APP/PS1 TRANSGENICAL MICE MODEL

2015 ◽  
pp. 1-6
Author(s):  
Y.-Q. Zeng ◽  
Y.-J. Wang ◽  
X.-F. Zhou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Biological Properties ◽  
Amyloid Angiopathy ◽  
Amyloid Beta Protein ◽  
Mice Model ◽  
Cerebral Microhemorrhage ◽  
The Brain

The extracellular accumulation of amyloid beta protein (Aβ), reactive gliosis and cerebral amyloid angiopathy (CAA) play critical roles in the pathogenesis of Alzheimer’s disease (AD). Ginkgetin, a biflavone isolated from Ginkgo biloba leaves, was previously reported to exhibit strong neuroprotection against cytotoxic insults induced by oxidative stress and amyloid beta, but it remains unclear whether ginkgetin has therapeutic effect on Alzheimer’s disease (AD) in vivo. In the present study, we investigated 9 months treatment effects of ginkgetin diet in APP/PS1 mice. Our results show that ginkgetin can significantly reduce plasma Aβ levels 59% and Aβ plaque 51% in the brain of APP/PS1 transgenic mice (P<0.05), effectively inhibits cerebral microhemorrhage 69% (P<0.05), significantly decreases astrogliosis 50% and ameliorate inflammation (P<0.05), exhibits several biological properties for AD.

scholarly journals Reelin delays amyloid-beta fibril formation and rescues cognitive deficits in a model of Alzheimer’s disease

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Lluís Pujadas ◽  
Daniela Rossi ◽  
Rosa Andrés ◽  
Cátia M. Teixeira ◽  
Bernat Serra-Vidal ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Cognitive Deficits ◽  
Fibril Formation ◽  
Model Of Alzheimer’S Disease

scholarly journals Amyloid Beta-Related Alterations to Glutamate Signaling Dynamics During Alzheimer’s Disease Progression

ASN NEURO ◽  
2019 ◽  
Vol 11 ◽  
pp. 175909141985554 ◽  
Author(s):  
Caleigh A. Findley ◽  
Andrzej Bartke ◽  
Kevin N. Hascup ◽  
Erin R. Hascup
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Progression ◽  
Amyloid Beta ◽  
Cognitive Deficits ◽  
Senile Plaques ◽  
Neuronal Loss ◽  
Long Term Potentiation ◽  
Term Potentiation

Alzheimer’s disease (AD) ranks sixth on the Centers for Disease Control and Prevention Top 10 Leading Causes of Death list for 2016, and the Alzheimer’s Association attributes 60% to 80% of dementia cases as AD related. AD pathology hallmarks include accumulation of senile plaques and neurofibrillary tangles; however, evidence supports that soluble amyloid beta (Aβ), rather than insoluble plaques, may instigate synaptic failure. Soluble Aβ accumulation results in depression of long-term potentiation leading to cognitive deficits commonly characterized in AD. The mechanisms through which Aβ incites cognitive decline have been extensively explored, with a growing body of evidence pointing to modulation of the glutamatergic system. The period of glutamatergic hypoactivation observed alongside long-term potentiation depression and cognitive deficits in later disease stages may be the consequence of a preceding period of increased glutamatergic activity. This review will explore the Aβ-related changes to the tripartite glutamate synapse resulting in altered cell signaling throughout disease progression, ultimately culminating in oxidative stress, synaptic dysfunction, and neuronal loss.

scholarly journals Glutaredoxin1 Diminishes Amyloid Beta-Mediated Oxidation of F-Actin and Reverses Cognitive Deficits in an Alzheimer's Disease Mouse Model

2019 ◽  
Vol 31 (18) ◽  
pp. 1321-1338 ◽  
Author(s):  
Reddy Peera Kommaddi ◽  
Deepika Singh Tomar ◽  
Smitha Karunakaran ◽  
Deepti Bapat ◽  
Siddharth Nanguneri ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Beta ◽  
Cognitive Deficits ◽  
Mediated Oxidation
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