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.

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 Leptin enhances adult neurogenesis and reduces pathological features in a transgenic mouse model of Alzheimer’s disease

2021 ◽  
Vol 148 ◽  
pp. 105219
Author(s):  
Michele Longoni Calió ◽  
Amanda Cristina Mosini ◽  
Darci Souza Marinho ◽  
Geisa Nogueira Salles ◽  
Fernando Henrique Massinhani ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Adult Neurogenesis ◽  
Transgenic Mouse Model ◽  
Pathological Features ◽  
Model Of Alzheimer’S Disease

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.

scholarly journals The NLRP3 inflammasome inhibitor OLT1177 rescues cognitive impairment in a mouse model of Alzheimer’s disease

2020 ◽  
Vol 117 (50) ◽  
pp. 32145-32154
Author(s):  
Niklas Lonnemann ◽  
Shirin Hosseini ◽  
Carlo Marchetti ◽  
Damaris B. Skouras ◽  
Davide Stefanoni ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Nlrp3 Inflammasome ◽  
Therapeutic Potential ◽  
Active Form ◽  
Specific Inhibitor ◽  
Morris Water Maze Test ◽  
Model Of Alzheimer’S Disease

Numerous studies demonstrate that neuroinflammation is a key player in the progression of Alzheimer’s disease (AD). Interleukin (IL)-1β is a main inducer of inflammation and therefore a prime target for therapeutic options. The inactive IL-1β precursor requires processing by the the nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome into a mature and active form. Studies have shown that IL-1β is up-regulated in brains of patients with AD, and that genetic inactivation of the NLRP3 inflammasome improves behavioral tests and synaptic plasticity phenotypes in a murine model of the disease. In the present study, we analyzed the effect of pharmacological inhibition of the NLRP3 inflammasome using dapansutrile (OLT1177), an oral NLRP3-specific inhibitor that is safe in humans. Six-month-old WT and APP/PS1 mice were fed with standard mouse chow or OLT1177-enriched chow for 3 mo. The Morris water maze test revealed an impaired learning and memory ability of 9-mo-old APP/PS1 mice (P = 0.001), which was completely rescued by OLT1177 fed to mice (P = 0.008 to untreated APP/PS1). Furthermore, our findings revealed that 3 mo of OLT1177 diet can rescue synaptic plasticity in this mouse model of AD (P = 0.007 to untreated APP/PS1). In addition, microglia were less activated (P = 0.07) and the number of plaques was reduced in the cortex (P = 0.03) following NLRP3 inhibition with OLT1177 administration. We also observed an OLT1177 dose-dependent normalization of plasma metabolic markers of AD to those of WT mice. This study suggests the therapeutic potential of treating neuroinflammation with an oral inhibitor of the NLRP3 inflammasome.

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