scholarly journals The 5XFAD Mouse Model of Alzheimer’s Disease Exhibits an Age-Dependent Increase in Anti-Ceramide IgG and Exogenous Administration of Ceramide Further Increases Anti-Ceramide Titers and Amyloid Plaque Burden

2015 ◽  
Vol 46 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Michael B. Dinkins ◽  
Somsankar Dasgupta ◽  
Guanghu Wang ◽  
Gu Zhu ◽  
Qian He ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Plaque ◽  
Plaque Burden ◽  
Model Of Alzheimer’S Disease ◽  
Age Dependent ◽  
5Xfad Mouse

scholarly journals Microglial-associated responses to comorbid amyloid pathology and hyperhomocysteinemia in an aged knock-in mouse model of Alzheimer’s disease

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
David J. Braun ◽  
Edgardo Dimayuga ◽  
Josh M. Morganti ◽  
Linda J. Van Eldik
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Inflammatory Responses ◽  
Specific Effect ◽  
Amyloid Plaque ◽  
Plaque Burden ◽  
Amyloid Pathology ◽  
Model Of Alzheimer’S Disease ◽  
B Vitamin

Abstract Background Elevated blood homocysteine levels, termed hyperhomocysteinemia (HHcy), is a prevalent risk factor for Alzheimer’s disease (AD) in elderly populations. While dietary supplementation of B-vitamins is a generally effective method to lower homocysteine levels, there is little if any benefit to cognition. In the context of amyloid pathology, dietary-induced HHcy is known to enhance amyloid deposition and certain inflammatory responses. Little is known, however, about whether there is a more specific effect on microglia resulting from combined amyloid and HHcy pathologies. Methods The present study used a knock-in mouse model of amyloidosis, aged to 12 months, given 8 weeks of B-vitamin deficiency-induced HHcy to better understand how microglia are affected in this comorbidity context. Results We found that HHcy-inducing diet increased amyloid plaque burden, altered the neuroinflammatory milieu, and upregulated the expression of multiple damage-associated and “homeostatic” microglial genes. Conclusions Taken together, these data indicate complex effects of comorbid pathologies on microglial function that are not driven solely by increased amyloid burden. Given the highly dynamic nature of microglia, their central role in AD pathology, and the frequent occurrence of various comorbidities in AD patients, it is increasingly important to understand how microglia respond to mixed pathological processes.

scholarly journals Exosome reduction in vivo is associated with lower amyloid plaque load in the 5XFAD mouse model of Alzheimer's disease

2014 ◽  
Vol 35 (8) ◽  
pp. 1792-1800 ◽  
Author(s):  
Michael B. Dinkins ◽  
Somsankar Dasgupta ◽  
Guanghu Wang ◽  
Gu Zhu ◽  
Erhard Bieberich
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Plaque ◽  
Model Of Alzheimer’S Disease ◽  
Plaque Load ◽  
5Xfad Mouse

scholarly journals Microglial-associated responses to comorbid amyloid pathology and hyperhomocysteinemia in an aged knock-in mouse model of Alzheimer’s disease

2020 ◽  
Author(s):  
David James Braun ◽  
Edgardo Dimayuga ◽  
Josh M. Morganti ◽  
Linda J Van Eldik
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Inflammatory Responses ◽  
Amyloid Plaque ◽  
Plaque Burden ◽  
Dynamic Nature ◽  
Amyloid Pathology ◽  
Specific Effects ◽  
Model Of Alzheimer’S Disease

Abstract Background: Elevated blood homocysteine levels, termed hyperhomocysteinemia (HHcy), is a prevalent risk factor for Alzheimer’s disease (AD) in elderly populations. While dietary supplementation of B-vitamins is a generally effective method to lower homocysteine levels, there is little if any benefit to cognition. In the context of amyloid pathology, dietary-induced HHcy is known to enhance amyloid deposition and certain inflammatory responses. Little is known, however, about the specific effects on microglia resulting from combined amyloid and HHcy pathologies. Methods: The present study used a knock-in mouse model of amyloidosis, aged to 12 months, given 8 weeks of dietary deficiency-induced HHcy to better understand how microglia are affected in this comorbidity context. Results: We found that HHcy-inducing diet increased amyloid plaque burden, altered the neuroinflammatory milieu, and upregulated the expression of multiple damage-associated and “homeostatic” microglial genes. Conclusions: Taken together, these data indicate complex effects of comorbid pathologies on microglial function that are not driven solely by increased amyloid burden. Given the highly dynamic nature of microglia, their central role in AD pathology, and the frequent occurrence of various comorbidities in AD patients, it is increasingly important to understand how microglia respond to mixed pathological processes.

scholarly journals Bacterial sepsis increases hippocampal fibrillar amyloid plaque load and neuroinflammation in a mouse model of Alzheimer's disease

2021 ◽  
Vol 152 ◽  
pp. 105292
Author(s):  
Jacob M. Basak ◽  
Aura Ferreiro ◽  
Lucy S. Cohen ◽  
Patrick W. Sheehan ◽  
Collin J. Nadarajah ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Plaque ◽  
Bacterial Sepsis ◽  
Model Of Alzheimer’S Disease ◽  
Plaque Load
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