scholarly journals Age-related increase in amyloid plaque burden is associated with impairment in conditioned fear memory in CRND8 mouse model of amyloidosis

2012 ◽  
Vol 4 (3) ◽  
pp. 21 ◽  
Author(s):  
Amanda Hanna ◽  
Kayleigh Iremonger ◽  
Pritam Das ◽  
Dennis Dickson ◽  
Todd Golde ◽  
...  
Keyword(s):  
Mouse Model ◽  
Conditioned Fear ◽  
Amyloid Plaque ◽  
Fear Memory ◽  
Plaque Burden ◽  
Age Related ◽  
Related Increase

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 Region-specific neuron and synapse loss in the hippocampus of APPSL/PS1 knock-in mice

2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Ivona Brasnjevic ◽  
Roy Lardenoije ◽  
Christoph Schmitz ◽  
Nicolien Kolk ◽  
Dara Dickstein ◽  
...  
Keyword(s):  
Amyloid Plaque ◽  
Aging Brain ◽  
Synapse Loss ◽  
Age Related ◽  
Plaque Load ◽  
Specific Accumulation ◽  
Aβ Aggregation ◽  
Presynaptic Boutons ◽  
Brain Age ◽  
Related Increase

AbstractTransgenic mouse models with knock-in (KI) expression of human mutant amyloid precursor protein (APP) and/or human presenilin 1 (PS1) may be helpful to elucidate the cellular consequences of APP and PS1 misprocessing in the aging brain. Age-related alterations in total numbers of neurons and in numbers of synaptophysin-immunoreactive presynaptic boutons (SIPB), as well as the amyloid plaque load were analyzed in the hippocampal dentate gyrus (DG), CA3, and CA1-2 of 2- and 10-month-old APPSL/PS1 homozygous KI, APPSL (expressing human mutant APP751 carrying the Swedish [K670N/M671L] and London [V717I] mutations under Thy-1 promoter), and PS1 homozygous KI mice (expressing human PS1 mutations [M233T and L235P]). APPSL/PS1 homozygous KI mice, but neither APPSL mice nor PS1 homozygous KI mice, showed substantial agerelated loss of neurons (−47.2%) and SIPB (−22.6%), specifically in CA1-2. PS1 homozygous KI mice showed an age-related increase in hippocampal granule cell numbers (+37.9%). Loss of neurons and SIPB greatly exceeded the amount of local extracellular Aβ aggregation and astrocytes, whereas region-specific accumulation of intraneuronal Aβ preceded neuron and synapse loss. An age-related increase in the ratio of SIPB to neuron numbers in CA1-2 of APPSL/PS1 homozygous KI mice was suggestive of compensatory synaptic plasticity. These findings indicate a region-selectivity in intra- and extraneuronal Aβ accumulation in connection with neuron and synapse loss in the hippocampus of APPSL/PS1 homozygous KI mice.

scholarly journals CR1is associated with amyloid plaque burden and age-related cognitive decline

2011 ◽  
Vol 69 (3) ◽  
pp. 560-569 ◽  
Author(s):  
Lori B. Chibnik ◽  
Joshua M. Shulman ◽  
Sue E. Leurgans ◽  
Julie A. Schneider ◽  
Robert S. Wilson ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Amyloid Plaque ◽  
Plaque Burden ◽  
Age Related ◽  
Age Related Cognitive Decline

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 Place cell firing correlates with memory deficits and amyloid plaque burden in Tg2576 Alzheimer mouse model

2008 ◽  
Vol 105 (22) ◽  
pp. 7863-7868 ◽  
Author(s):  
F. Cacucci ◽  
M. Yi ◽  
T. J. Wills ◽  
P. Chapman ◽  
J. O'Keefe
Keyword(s):  
Mouse Model ◽  
Amyloid Plaque ◽  
Memory Deficits ◽  
Place Cell ◽  
Plaque Burden ◽  
Cell Firing ◽  
With Memory

scholarly journals Striking reduction of amyloid plaque burden in an Alzheimer's mouse model after chronic administration of carmustine

BMC Medicine ◽  
2013 ◽  
Vol 11 (1) ◽  
Author(s):  
Crystal D Hayes ◽  
Debleena Dey ◽  
Juan Pablo Palavicini ◽  
Hongjie Wang ◽  
Kshitij A Patkar ◽  
...  
Keyword(s):  
Mouse Model ◽  
Chronic Administration ◽  
Amyloid Plaque ◽  
Plaque Burden
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