Memory Function in a Mouse Genetic Model of Alzheimer's Disease

2011 ◽  
Vol 25 (3) ◽  
pp. 433-444 ◽  
Author(s):  
Avdesh Avdesh ◽  
Patrick Wong ◽  
Ralph N. Martins ◽  
Mathew T. Martin-Iverson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Model ◽  
Memory Function ◽  
Model Of Alzheimer’S Disease ◽  
Mouse Genetic Model ◽  
Mouse Genetic

scholarly journals Increasing cerebral blood flow improves cognition into late stages in Alzheimer’s disease mice

2019 ◽  
Vol 40 (7) ◽  
pp. 1441-1452 ◽  
Author(s):  
Oliver Bracko ◽  
Brendah N Njiru ◽  
Madisen Swallow ◽  
Muhammad Ali ◽  
Mohammad Haft-Javaherian ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Short Term Memory ◽  
Memory Function ◽  
Neutrophil Adhesion ◽  
Short Term ◽  
Term Memory ◽  
Model Of Alzheimer’S Disease

Alzheimer’s disease is associated with a 20–30% reduction in cerebral blood flow. In the APP/PS1 mouse model of Alzheimer’s disease, inhibiting neutrophil adhesion using an antibody against the neutrophil specific protein Ly6G was recently shown to drive rapid improvements in cerebral blood flow that was accompanied by an improvement in performance on short-term memory tasks. Here, in a longitudinal aging study, we assessed how far into disease development a single injection of anti-Ly6G treatment can acutely improve short-term memory function. We found that APP/PS1 mice as old as 15–16 months had improved performance on the object replacement and Y-maze tests of spatial and working short-term memory, measured at one day after anti-Ly6G treatment. APP/PS1 mice at 17–18 months of age or older did not show acute improvements in cognitive performance, although we did find that capillary stalls were still reduced and cerebral blood flow was still increased by 17% in 21–22-months-old APP/PS1 mice given anti-Ly6G antibody. These data add to the growing body of evidence suggesting that cerebral blood flow reductions are an important contributing factor to the cognitive dysfunction associated with neurodegenerative disease. Thus, interfering with neutrophil adhesion could be a new therapeutic approach for Alzheimer’s disease.

Metformin Treatment Alters Memory Function in a Mouse Model of Alzheimer's Disease

2015 ◽  
Vol 44 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Kacee A. DiTacchio ◽  
Stephen F. Heinemann ◽  
Gustavo Dziewczapolski
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Memory Function ◽  
Metformin Treatment ◽  
Model Of Alzheimer’S Disease

scholarly journals Adrenergic mechanisms of myocardium contractility regulation in genetic model of Alzheimer’s disease

2015 ◽  
Vol 96 (1) ◽  
pp. 50-55 ◽  
Author(s):  
A V Leushina ◽  
L F Nurullin ◽  
E O Petukhova ◽  
A L Zefirov ◽  
M A Mukhamedyarov
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Adrenergic Receptors ◽  
Myocardial Contractility ◽  
Genetic Model ◽  
Immunofluorescent Staining ◽  
Wild Type ◽  
Adrenergic Mechanisms ◽  
Model Of Alzheimer’S Disease

Aim. Study is aimed to investigate contractility impairments and receptor mechanisms of adrenergic regulation of myocardium inotropic function in Alzheimer’s disease model on transgenic mice.Methods. Experiments were performed on isolated preparations of atria and ventricles myocardium of mice. Transgenic mice of B6C3-Tg(APP695)85Dbo Tg(PSENI)85Dbo genotype were used as animal model of Alzheimer’s disease. Contractile responses of myocardium were registered by conventional myographic technique in isometric conditions. To evaluate the expression of adrenergic receptors, immunofluorescence staining of myocardium with specific antibodies was performed.Results. Transgenic mice showed not only a decreased effect of norepinephrine on myocardium inotropic function but also the inversion of the effect of norepinephrine - the use of 10-5-10-4 M of norepinephrine decreased myocardium inotropic function. Immunofluorescent staining showed decrease of expression of β1- and especially β2-adrenergic receptors ventricular myocardium of transgenic mice comparing to wild type mice. Adrenergic deregulation was registered in ventricles, but not in atria. The features of adrenergic regulatory mechanisms of myocardial contractility in transgenic APP/PS1 mice aged 8-10 months are specific, although somewhat similar to wild type mice aged 8-10 months, and are evidently due to Alzheimer’s disease. The inversion of norepinephrine inotropic effect (from positive to negative) may be explained by switching the intracellular cascade pathway of β2-adrenergic receptors effects to another type of G-protein.Conclusion. The results indicate that peripheral adrenergic mechanisms of myocardial contractility regulation are impaired in studied transgenic mice model of Alzheimer’s disease. Obtained data widen our understanding of Alzheimer’s disease pathogenesis, as well as our conception of relations between cardiovascular diseases and neurodegeneration.

Ca2+-permeable TRPV1 pain receptor knockout rescues memory deficits and reduces amyloid-β and tau in a mouse model of Alzheimer’s disease

2019 ◽  
Vol 29 (2) ◽  
pp. 228-237 ◽  
Author(s):  
Juyong Kim ◽  
Siyoung Lee ◽  
Jaekyoon Kim ◽  
Sangwoo Ham ◽  
Jung Han Yoon Park ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nervous System ◽  
Mouse Model ◽  
Transient Receptor Potential ◽  
Memory Function ◽  
Amyloid Β ◽  
Neuronal Cultures ◽  
Transient Receptor Potential Vanilloid ◽  
Model Of Alzheimer’S Disease

Abstract The transient receptor potential vanilloid 1 (TRPV1) protein is a pain receptor that elicits a hot sensation when an organism eats the capsaicin of red chili peppers. This calcium (Ca2+)-permeable cation channel is mostly expressed in the peripheral nervous system sensory neurons but also in the central nervous system (e.g. hippocampus and cortex). Preclinical studies found that TRPV1 mediates behaviors associated with anxiety and depression. Loss of TRPV1 functionality increases expression of genes related to synaptic plasticity and neurogenesis. Thus, we hypothesized that TRPV1 deficiency may modulate Alzheimer’s disease (AD). We generated a triple-transgenic AD mouse model (3xTg-AD+/+) with wild-type (TRPV1+/+), hetero (TRPV1+/−) and knockout (TRPV1−/−) TRPV1 to investigate the role of TRPV1 in AD pathogenesis. We analyzed the animals’ memory function, hippocampal Ca2+ levels and amyloid-β (Aβ) and tau pathologies when they were 12 months old. We found that compared with 3xTg-AD−/−/TRPV1+/+ mice, 3xTg-AD+/+/TRPV1+/+ mice had memory impairment and increased levels of hippocampal Ca2+, Aβ and total and phosphorylated tau. However, 3xTg-AD+/+/TRPV1−/− mice had better memory function and lower levels of hippocampal Ca2+, Aβ, tau and p-tau, compared with 3xTg-AD+/+/TRPV1+/+ mice. Examination of 3xTg-AD-derived primary neuronal cultures revealed that the intracellular Ca2+ chelator BAPTA/AM and the TRPV1 antagonist capsazepine decreased the production of Aβ, tau and p-tau. Taken together, these results suggested that TRPV1 deficiency had anti-AD effects and promoted resilience to memory loss. These findings suggest that drugs or food components that modulate TRPV1 could be exploited as therapeutics to prevent or treat AD.

Region- and age-dependent reductions of hippocampal long-term potentiation and NMDA to AMPA ratio in a genetic model of Alzheimer's disease

2015 ◽  
Vol 36 (1) ◽  
pp. 123-133 ◽  
Author(s):  
Alessandro Tozzi ◽  
Alessandra Sclip ◽  
Michela Tantucci ◽  
Antonio de Iure ◽  
Veronica Ghiglieri ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Model ◽  
Long Term Potentiation ◽  
Model Of Alzheimer’S Disease ◽  
Term Potentiation ◽  
Age Dependent

scholarly journals Administration of Bifidobacterium bifidum BGN4 and Bifidobacterium longum BORI Improves Cognitive and Memory Function in the Mouse Model of Alzheimer’s Disease

2021 ◽  
Vol 13 ◽  
Author(s):  
Hongwon Kim ◽  
Sumin Kim ◽  
Sang-jun Park ◽  
Gwoncheol Park ◽  
Hakdong Shin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Therapeutic Potential ◽  
Memory Function ◽  
Bifidobacterium Longum ◽  
Bifidobacterium Bifidum ◽  
Pathological Features ◽  
Bdnf Expression ◽  
Model Of Alzheimer’S Disease

Recent evidence indicates that gut microbiota could interact with the central nervous system and affect brain function, including cognition and memory. In this study, we investigated whether Bifidobacterium bifidum BGN4 (B. bifidum BGN4) and Bifidobacterium longum BORI (B. longum BORI) alleviated the pathological features in a mouse model of Alzheimer’s disease (AD). Administration of B. bifidum BGN4 and B. longum BORI effectively suppressed amyloidosis and apoptotic processes and improved synaptic plasticity by ameliorating the neuroinflammatory response and BDNF expression. Moreover, behavioral tests indicated that B. bifidum BGN4 and B. longum BORI attenuated the cognitive and memory disability of AD mice. Taken together, the present study highlights the therapeutic potential of B. bifidum BGN4 and B. longum BORI for suppressing the pathological features of AD.

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