Progranulin expression correlates with dense-core amyloid plaque burden in Alzheimer disease mouse models

2009 ◽  
Vol 219 (2) ◽  
pp. 173-181 ◽  
Author(s):  
Sandra Pereson ◽  
Hans Wils ◽  
Gernot Kleinberger ◽  
Eileen McGowan ◽  
Mado Vandewoestyne ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Mouse Models ◽  
Amyloid Plaque ◽  
Dense Core ◽  
Plaque Burden

Loss of GPR3 reduces the amyloid plaque burden and improves memory in Alzheimer’s disease mouse models

2015 ◽  
Vol 7 (309) ◽  
pp. 309ra164-309ra164 ◽  
Author(s):  
Yunhong Huang ◽  
Aneta Skwarek-Maruszewska ◽  
Katrien Horré ◽  
Elke Vandewyer ◽  
Leen Wolfs ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Models ◽  
Amyloid Plaque ◽  
Plaque Burden

scholarly journals Detection of Alzheimer Disease Pathology in Patients Using Biochemical Biomarkers: Prospects and Challenges for Use in Clinical Practice

2019 ◽  
Vol 5 (1) ◽  
pp. 183-193 ◽  
Author(s):  
Leslie M Shaw ◽  
Magdalena Korecka ◽  
Michal Figurski ◽  
Jon Toledo ◽  
David Irwin ◽  
...  
Keyword(s):  
Clinical Practice ◽  
Alzheimer Disease ◽  
Clinical Utility ◽  
Amyloid Β ◽  
Amyloid Plaque ◽  
Plaque Burden ◽  
Appropriate Use ◽  
Tangle Pathology ◽  
Disease Modifying Agents ◽  
Τ Protein

Abstract Background Thirty-four years ago, amyloid-β 1-42 peptide was identified in amyloid plaques from brain tissue obtained from patients with Alzheimer disease (AD) and Down syndrome. This finding led to development of immunoassays for this marker of amyloid plaque burden in cerebrospinal fluid (CSF) approximately 10 years later. Subsequently, research immunoassays were developed for total τ protein and τ phosphorylated at the threonine 181 position. Subsequent studies documented the clinical utility of these biomarkers of amyloid plaque burden or τ tangle pathology in cohorts of living patients. Content We describe the following: (a) clinical utility of AD biomarkers; (b) measurement challenges, including development of mass spectrometry-based reference methods and automated immunoassays; (c) development of “appropriate use criteria” (AUC) guidelines for safe/appropriate use of CSF testing for diagnosis of AD developed by neurologists, a neuroethicist, and laboratorians; (d) a framework, sponsored by the National Institute of Aging-Alzheimer's Association (NIA-AA), that defines AD on the basis of CSF and imaging methods for detecting amyloid plaque burden, τ tangle pathology, and neurodegeneration. This framework's purpose was investigative but has important implications for future clinical practice; (e) recognition of copathologies in AD patients and challenges for developing methods to detect these in living patients. Summary The field can expect availability of validated research tools for detection of AD pathology that support clinical treatment trials of disease-modifying agents and, ultimately, use in clinical practice. Validated methods are becoming available for CSF testing; emergence of validated methods for AD biomarkers in plasma can be expected in the next few years.

scholarly journals Reducing Amyloid Plaque Burden via Ex Vivo Gene Delivery of an Aβ-Degrading Protease: A Novel Therapeutic Approach to Alzheimer Disease

PLoS Medicine ◽  
2007 ◽  
Vol 4 (8) ◽  
pp. e262 ◽  
Author(s):  
Matthew L Hemming ◽  
Michaela Patterson ◽  
Casper Reske-Nielsen ◽  
Ling Lin ◽  
Ole Isacson ◽  
...  
Keyword(s):  
Gene Delivery ◽  
Alzheimer Disease ◽  
Therapeutic Approach ◽  
Ex Vivo ◽  
Amyloid Plaque ◽  
Plaque Burden ◽  
Novel Therapeutic

O1-03-07: Progranulin correlates with dense-core plaque burden in Alzheimer's disease mouse models

2009 ◽  
Vol 5 (4S_Part_3) ◽  
pp. P83-P83
Author(s):  
Sandra Pereson ◽  
Gernot Kleinberger ◽  
Hans Wils ◽  
Eileen McGowan ◽  
Mathias Jucker ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Models ◽  
Dense Core ◽  
Plaque Burden

Asymmetry of plaque burden in amyloid mouse models

2020 ◽  
Author(s):  
L Beyer ◽  
C Sacher ◽  
T Blume ◽  
J Sauerbeck ◽  
F Eckenweber ◽  
...  
Keyword(s):  
Mouse Models ◽  
Plaque Burden

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 Age-Related Changes of the Neurovascular Unit in the Cerebral Cortex of Alzheimer Disease Mouse Models: A Neuroanatomical and Molecular Study

2019 ◽  
Vol 78 (2) ◽  
pp. 101-112 ◽  
Author(s):  
Alessandro Giuliani ◽  
Sandra Sivilia ◽  
Vito Antonio Baldassarro ◽  
Marco Gusciglio ◽  
Luca Lorenzini ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Alzheimer Disease ◽  
Mouse Models ◽  
Neurovascular Unit ◽  
Molecular Study ◽  
Age Related ◽  
Age Related Changes
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