scholarly journals Early Intervention with an Estrogen Receptor β-Selective Phytoestrogenic Formulation Prolongs Survival, Improves Spatial Recognition Memory, and Slows Progression of Amyloid Pathology in a Female Mouse Model of Alzheimer's Disease

2013 ◽  
Vol 37 (2) ◽  
pp. 403-419 ◽  
Author(s):  
Liqin Zhao ◽  
Zisu Mao ◽  
Shuhua Chen ◽  
Lon S. Schneider ◽  
Roberta D. Brinton
Keyword(s):  
Alzheimer’S Disease ◽  
Estrogen Receptor ◽  
Early Intervention ◽  
Recognition Memory ◽  
Mouse Model ◽  
Female Mouse ◽  
Estrogen Receptor Β ◽  
Amyloid Pathology ◽  
Model Of Alzheimer’S Disease ◽  
Spatial Recognition

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.

P1-204: DELETION OF A SINGLE BIN1 ALLELE DOES NOT ALTER AMYLOID PATHOLOGY IN A MOUSE MODEL OF ALZHEIMER'S DISEASE

2006 ◽  
Vol 14 (7S_Part_6) ◽  
pp. P358-P358
Author(s):  
Robert J. Andrew ◽  
Pierre De Rossi ◽  
Thomas Guerbette ◽  
Sofia V. Krause ◽  
Richard C. Rice ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Pathology ◽  
Model Of Alzheimer’S Disease
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