scholarly journals Studying the Relationship of Intermittent Fasting and β-Amyloid in Animal Model of Alzheimer’s Disease: A Scoping Review

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3215
Author(s):  
Muhammad Luqman Nasaruddin ◽  
Syarifah Aisyah Syed Abd Halim ◽  
Mohd Amir Kamaruzzaman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Dietary Habits ◽  
Longitudinal Research ◽  
Intermittent Fasting ◽  
Restricted Feeding ◽  
Model Of Alzheimer’S Disease ◽  
Alternate Day Fasting ◽  
Β Amyloid

We examined the evidence for intermittent fasting (IF) as a preventative tool to influence β-amyloid in animal models of Alzheimer’s disease (AD). A Scopus, Ovid, PubMed, and Web of Science (WoS), search yielded 29 results using the keywords “amyloid beta”, “intermittent fasting”, “intermittent caloric restriction”, “alternate day fasting”, “modified alternate-day fasting”, “time-restricted feeding”, “Ramadan fast”, “intermittent calori* restriction”, “intermittent restrictive diet”, and “Alzheimer*”. Five research articles addressed directly the effects of intermittent fasting on β-amyloid levels in animal models of AD: alternate day fasting (ADF) and time-restricted feeding (TRF) methods were incorporated in these studies. The study designs were found to be heterogeneous. Variations in the levels of β-amyloid peptides or plaque in either the hippocampus, cortical areas, or both in animals following dietary intervention were observed as compared to the ad libitum group. Non-significant changes were observed in three studies, while two studies interestingly demonstrated amelioration and reduction in β-amyloid levels. Given the conflicting results obtained from this study, significant care has to be taken into consideration before the protocol can be applied as a preventative approach to treat Alzheimer’s disease. Longitudinal research is warranted to fully grasp how dietary habits can help alleviate the disease either through upstream or downstream of AD pathology.

scholarly journals P3-270: CHF5074 reduces brain β-amyloid burden and hyperphosphorylated tau in a mouse model of Alzheimer's disease

2009 ◽  
Vol 5 (4S_Part_14) ◽  
pp. P422-P422
Author(s):  
M. Pizzi ◽  
A. Lanzillotta ◽  
B.P. Imbimbo ◽  
B. Hutter-Paier ◽  
G. Villetti ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Hyperphosphorylated Tau ◽  
Amyloid Burden ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

The β-Amyloid Model of Alzheimer’s Disease

1997 ◽  
pp. 73-90 ◽  
Author(s):  
Carl W. Cotman ◽  
David H. Cribbs ◽  
Aileen J. Anderson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

scholarly journals Microglial and Astrocyte priming in the APP/PS1 model of Alzheimer’s Disease: increased vulnerability to acute inflammation and cognitive deficits

2018 ◽  
Author(s):  
Ana Belen Lopez-Rodriguez ◽  
Edel Hennessy ◽  
Carol Murray ◽  
Anouchka Lewis ◽  
Niamh de Barra ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficits ◽  
Inflammasome Activation ◽  
Nuclear Localisation ◽  
Amyloid Pathology ◽  
Model Of Alzheimer’S Disease ◽  
Nlrp3 Inflammasome Activation ◽  
Β Amyloid ◽  
Secondary Stimulation

AbstractAlzheimer’s disease (AD) causes devastating cognitive decline and has no disease-modifying therapies. Neuroinflammation is a significant contributor to disease progression but its precise contribution remains unclear. An emerging literature indicates that secondary inflammatory insults including acute trauma and infection alter the trajectory of chronic neurodegenerative diseases and the roles of microglia and astrocytes require elucidation. The current study, using the APP/PS1 mouse model of AD, demonstrates that microglia are primed by β-amyloid pathology to induce exaggerated IL-1β responses to acute stimulation with LPS or IL-1β. Despite disease-associated NLRP3 inflammasome activation, evidenced by ASC speck formation, APP/PS1 microglial cells show neither IL-1β induction nor NFκB p65 nuclear localisation. Upon secondary stimulation with LPS or IL-1β, NFκB-p65 nuclear localisation and exaggerated pro-IL-1 induction occur. Microglial priming was also unmasked by secondary stimulation with systemic LPS leading to significant cognitive impairment in APP/PS1 mice compared to WT LPS-treated mice. Astrocytes have also recently emerged as displaying significant phenotypic heterogeneity. Here, by-passing microglial priming, and acutely challenging mice with intra-hippocampal IL-1β we demonstrate that astrocytes proximal to Aβ-plaques are also primed to produce exaggerated CCL2, CXCL1 and CXCL10 responses. Many astrocytosis-associated genes in APP/PS1 mice share these exaggerated responses to IL-1β, while others are equally induced in both strains. Collectively the data show that the amyloid-laden brain shows multiple vulnerabilities to secondary inflammatory challenge: both microglia and astrocytes are primed to produce exaggerated secondary inflammation and systemic LPS is sufficient to cause cognitive impairments relevant to delirium, selectively in animals with prior amyloid pathology.

scholarly journals PROTECTIVE EFFECT OF IRIS GERMANICA L. IN Β-AMYLOID-INDUCED ANIMAL MODEL OF ALZHEIMER’S DISEASE

2017 ◽  
Vol 14 (4) ◽  
pp. 140-148 ◽  
Author(s):  
Mona Borhani ◽  
Mohammad Sharifzadeh ◽  
Mohammad Hosein Farzaei ◽  
Zahra Narimani ◽  
Fatemeh Sabbaghziarani ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Protective Effect ◽  
Model Of Alzheimer’S Disease ◽  
Iris Germanica ◽  
Β Amyloid

scholarly journals A ketogenic diet improves motor performance but does not affect β-amyloid levels in a mouse model of Alzheimer's Disease

2013 ◽  
Vol 1505 ◽  
pp. 61-67 ◽  
Author(s):  
Tina L. Beckett ◽  
Christa M. Studzinski ◽  
Jeffrey N. Keller ◽  
M. Paul Murphy ◽  
Dana M. Niedowicz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Ketogenic Diet ◽  
Motor Performance ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid
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