scholarly journals IFN-γ Promotes Complement Expression and Attenuates Amyloid Plaque Deposition in Amyloid β Precursor Protein Transgenic Mice

2010 ◽  
Vol 184 (9) ◽  
pp. 5333-5343 ◽  
Author(s):  
Paramita Chakrabarty ◽  
Carolina Ceballos-Diaz ◽  
Amanda Beccard ◽  
Christopher Janus ◽  
Dennis Dickson ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Β ◽  
Amyloid Plaque ◽  
Precursor Protein ◽  
Plaque Deposition ◽  
Ifn Γ

scholarly journals Neuroprotective Effects of Asparagus officinalis Stem Extract in Transgenic Mice Overexpressing Amyloid Precursor Protein

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zhanglong Peng ◽  
Supinder Bedi ◽  
Vivek Mann ◽  
Alamelu Sundaresan ◽  
Kohei Homma ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Caspase 3 ◽  
Amyloid Β ◽  
Precursor Protein ◽  
Tau Proteins ◽  
Asparagus Officinalis ◽  
Mouse Strains ◽  
Neuroprotective Effects ◽  
Shock Proteins

To mimic Alzheimer’s disease, transgenic mice overexpressing the amyloid precursor protein (APP) were used in this study. We hypothesize that the neuroprotective effects of ETAS®50, a standardized extract of Asparagus officinalis stem produced by Amino Up Co., Ltd. (Sapporo, Japan), are linked to the inhibition of the apoptosis cascade through an enhancement of the stress-response proteins: heat shock proteins (HSPs). APP-overexpressing mice (double-transgenic APP and PS1 mouse strains with a 129s6 background), ages 6-8 weeks old, and weighing 20-24 grams were successfully bred in our laboratory. The animals were divided into 5 groups. APP-overexpressing mice and wild-type (WT) mice were pretreated with ETAS®50 powder (50% elemental ETAS and 50% destrin) at 200 mg/kg and 1000 mg/kg body weight. Saline, the vehicle for ETAS®50, was administered in APP-overexpressing mice and WT mice. ETAS®50 and saline were administered by gavage daily for 1 month. Cognitive assessments, using the Morris Water Maze, demonstrated that memory was recovered following ETAS®50 treatment as compared to nontreated APP mice. At euthanization, the brain was removed and HSPs, amyloid β, tau proteins, and caspase-3 were evaluated through immunofluorescence staining with the appropriate antibodies. Our data indicate that APP mice have cognitive impairment along with elevated amyloid β, tau proteins, and caspase-3. ETAS®50 restored cognitive function in these transgenic mice, increased both HSP70 and HSP27, and attenuated pathogenic level of amyloid β, tau proteins, and caspsase-3 leading to neuroprotection. Our results were confirmed with a significant increase in HSP70 gene expression in the hippocampus.

scholarly journals Altered glycosylation of acetylcholinesterase in APP (SW) Tg2576 transgenic mice occurs prior to amyloid plaque deposition

2002 ◽  
Vol 81 (3) ◽  
pp. 441-448 ◽  
Author(s):  
Lisa R. Fodero ◽  
Javier Sáez-Valero ◽  
Catriona A. McLean ◽  
Ralph N. Martins ◽  
Konrad Beyreuther ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Plaque ◽  
Plaque Deposition ◽  
Altered Glycosylation

scholarly journals Regulation of amyloid-β dynamics and pathology by the circadian clock

2018 ◽  
Vol 215 (4) ◽  
pp. 1059-1068 ◽  
Author(s):  
Geraldine J. Kress ◽  
Fan Liao ◽  
Julie Dimitry ◽  
Michelle R. Cedeno ◽  
Garret A. FitzGerald ◽  
...  
Keyword(s):  
Circadian Rhythms ◽  
Circadian Clock ◽  
Amyloid Β ◽  
Amyloid Plaque ◽  
Brain Parenchyma ◽  
Targeted Deletion ◽  
Plaque Deposition ◽  
The Brain ◽  
Core Clock Gene

Nighttime restlessness and daytime drowsiness are common and early symptoms of Alzheimer’s Disease (AD). This symptomology implicates dysfunctional biological timing, yet the role of the circadian system in AD pathogenesis is unknown. To evaluate the role of the circadian clock in amyloid-β (Aβ) dynamics and pathology, we used a mouse model of β-amyloidosis and disrupted circadian clock function either globally or locally in the brain via targeted deletion of the core clock gene Bmal1. Our results demonstrate that loss of central circadian rhythms leads to disruption of daily hippocampal interstitial fluid Aβ oscillations and accelerates amyloid plaque accumulation, whereas loss of peripheral Bmal1 in the brain parenchyma increases expression of Apoe and promotes fibrillar plaque deposition. These results provide evidence that both central circadian rhythms and local clock function influence Aβ dynamics and plaque formation and demonstrate mechanisms by which poor circadian hygiene may directly influence AD pathogenesis.

scholarly journals The Neuronal Adaptor Protein X11β Reduces Amyloid β-Protein Levels and Amyloid Plaque Formation in the Brains of Transgenic Mice

2004 ◽  
Vol 279 (47) ◽  
pp. 49099-49104 ◽  
Author(s):  
Ju-Hyun Lee ◽  
Kwok-Fai Lau ◽  
Michael S. Perkinton ◽  
Claire L. Standen ◽  
Boris Rogelj ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Β ◽  
Adaptor Protein ◽  
Amyloid Plaque ◽  
Plaque Formation ◽  
Amyloid Β Protein ◽  
Protein Levels ◽  
Β Protein
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