scholarly journals Powerful beneficial effects of benfotiamine on cognitive impairment and  -amyloid deposition in amyloid precursor protein/presenilin-1 transgenic mice

Brain ◽  
2010 ◽  
Vol 133 (5) ◽  
pp. 1342-1351 ◽  
Author(s):  
X. Pan ◽  
N. Gong ◽  
J. Zhao ◽  
Z. Yu ◽  
F. Gu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Amyloid Deposition ◽  
Precursor Protein ◽  
Presenilin 1 ◽  
Beneficial Effects

scholarly journals Increased Extracellular Amyloid Deposition and Neurodegeneration in Human Amyloid Precursor Protein Transgenic Mice Deficient in Receptor-Associated Protein

2002 ◽  
Vol 22 (21) ◽  
pp. 9298-9304 ◽  
Author(s):  
Emily Van Uden ◽  
Margaret Mallory ◽  
Isaac Veinbergs ◽  
Michael Alford ◽  
Edward Rockenstein ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Amyloid Deposition ◽  
Precursor Protein ◽  
Receptor Associated Protein

scholarly journals Early-onset Amyloid Deposition and Cognitive Deficits in Transgenic Mice Expressing a Double Mutant Form of Amyloid Precursor Protein 695

2001 ◽  
Vol 276 (24) ◽  
pp. 21562-21570 ◽  
Author(s):  
M. Azhar Chishti ◽  
Dun-Shen Yang ◽  
Christopher Janus ◽  
Amie L. Phinney ◽  
Patrick Horne ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Cognitive Deficits ◽  
Early Onset ◽  
Double Mutant ◽  
Amyloid Deposition ◽  
Precursor Protein ◽  
Mutant Form

scholarly journals Vitamin A Deficiency Exacerbates Gut Microbiota Dysbiosis and Cognitive Deficits in Amyloid Precursor Protein/Presenilin 1 Transgenic Mice

2021 ◽  
Vol 13 ◽  
Author(s):  
Bo-Wen Chen ◽  
Kai-Wen Zhang ◽  
Si-Jia Chen ◽  
Chun Yang ◽  
Peng-Gao Li
Keyword(s):  
Cognitive Function ◽  
Vitamin A ◽  
Gut Microbiota ◽  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Intestinal Microbiota ◽  
Gaba Receptors ◽  
Vitamin A Deficiency ◽  
Precursor Protein ◽  
Presenilin 1

Vitamin A deficiency (VAD) plays an essential role in the pathogenesis of Alzheimer’s disease (AD). However, the specific mechanism by which VAD aggravates cognitive impairment is still unknown. At the intersection of microbiology and neuroscience, the gut-brain axis is undoubtedly contributing to the formation and function of neurological systems, but most of the previous studies have ignored the influence of gut microbiota on the cognitive function in VAD. Therefore, we assessed the effect of VAD on AD pathology and the decline of cognitive function in AD model mice and determined the role played by the intestinal microbiota in the process. Twenty 8-week-old male C57BL/6J amyloid precursor protein/presenilin 1 (APP/PS1) transgenic mice were randomly assigned to either a vitamin A normal (VAN) or VAD diet for 45 weeks. Our results show that VAD aggravated the behavioral learning and memory deficits, reduced the retinol concentration in the liver and the serum, decreased the transcription of vitamin A (VA)-related receptors and VA-related enzymes in the cortex, increased amyloid-β peptides (Aβ40 and Aβ42) in the brain and gut, upregulate the translation of beta-site APP-cleaving enzyme 1 (BACE1) and phosphorylated Tau in the cortex, and downregulate the expression of brain-derived neurotrophic factor (BDNF) and γ-aminobutyric acid (GABA) receptors in the cortex. In addition, VAD altered the composition and functionality of the fecal microbiota as exemplified by a decreased abundance of Lactobacillus and significantly different α- and β-diversity. Of note, the functional metagenomic prediction (PICRUSt analysis) indicated that GABAergic synapse and retinol metabolism decreased remarkably after VAD intervention, which was in line with the decreased expression of GABA receptors and the decreased liver and serum retinol. In summary, the present study provided valuable facts that VAD exacerbated the morphological, histopathological, molecular biological, microbiological, and behavioral impairment in the APP/PS1 transgenic mice, and the intestinal microbiota may play a key mediator role in this mechanism.

Reelin in plaques of β-amyloid precursor protein and presenilin-1 double-transgenic mice

2001 ◽  
Vol 316 (3) ◽  
pp. 145-148 ◽  
Author(s):  
Oliver Wirths ◽  
Gerd Multhaup ◽  
Christian Czech ◽  
Véronique Blanchard ◽  
Günter Tremp ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Precursor Protein ◽  
Presenilin 1 ◽  
Β Amyloid ◽  
Double Transgenic Mice

Central cholinergic functions in human amyloid precursor protein knock-in/presenilin-1 transgenic mice

Neuroscience ◽  
2004 ◽  
Vol 125 (4) ◽  
pp. 1009-1017 ◽  
Author(s):  
J Hartmann ◽  
C Erb ◽  
U Ebert ◽  
K.H Baumann ◽  
A Popp ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Precursor Protein ◽  
Presenilin 1

Transgenic mouse models of Alzheimer's disease: phenotype and mechanisms of pathogenesis

2001 ◽  
Vol 67 ◽  
pp. 195-202 ◽  
Author(s):  
Karen Duff
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Precursor Protein ◽  
Transgenic Mouse Models ◽  
Disease Phenotype

A range of transgenic mice have been created to model Alzheimer's disease. These include mice expressing human forms of the amyloid precursor protein, the presenilins and, more recently, tau. Several of the models develop features of the disease including amyloid pathology, cholinergic deficits, neurodegeneration and cognitive impairment. Progress in the characterization and use of these model animals is discussed.

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