P3-012: Immunochemical analysis of advanced glycation endproducts and amyloid in Alzheimer's disease and diabetic post-mortem brain tissue

2008 ◽  
Vol 4 ◽  
pp. T520-T520
Author(s):  
Alejandro Gella ◽  
Tony Valente ◽  
Mercedes Unzeta ◽  
Xavier Fernandez-Busquets ◽  
Nuria Durany
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Tissue ◽  
Advanced Glycation Endproducts ◽  
Immunochemical Analysis ◽  
Post Mortem ◽  
Advanced Glycation ◽  
Glycation Endproducts ◽  
Post Mortem Brain

P1-155: Post-Mortem Brain Tissue Characterisation of Inflammatory and Pathological Hallmarks of Alzheimer’s Disease During Disease Progression

2016 ◽  
Vol 12 ◽  
pp. P462-P462
Author(s):  
Martina M. Hughes ◽  
Beatriz G. Perez-Nievas ◽  
Claire Troakes ◽  
Michael Perkinton ◽  
Diane P. Hanger ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Progression ◽  
Brain Tissue ◽  
Post Mortem ◽  
Tissue Characterisation ◽  
Post Mortem Brain

scholarly journals Natriuretic Peptides in Post-mortem Brain Tissue and Cerebrospinal Fluid of Non-demented Humans and Alzheimer’s Disease Patients

2018 ◽  
Vol 12 ◽  
Author(s):  
Simin Mahinrad ◽  
Marjolein Bulk ◽  
Isabelle van der Velpen ◽  
Ahmed Mahfouz ◽  
Willeke van Roon-Mom ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Natriuretic Peptides ◽  
Post Mortem ◽  
Post Mortem Brain

scholarly journals Molecular signatures in post-mortem brain tissue of younger individuals at high risk for Alzheimer's disease as based on APOE genotype

2010 ◽  
Vol 16 (8) ◽  
pp. 836-847 ◽  
Author(s):  
C Conejero-Goldberg ◽  
T M Hyde ◽  
S Chen ◽  
U Dreses-Werringloer ◽  
M M Herman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
High Risk ◽  
Brain Tissue ◽  
Apoe Genotype ◽  
Molecular Signatures ◽  
Post Mortem ◽  
Post Mortem Brain

DEVELOPMENT OF AZELIRAGON, AN ORAL SMALL MOLECULE ANTAGONIST OF THE RECEPTOR FOR ADVANCED GLYCATION ENDPRODUCTS, FOR THE POTENTIAL SLOWING OF LOSS OF COGNITION IN MILD ALZHEIMER’S DISEASE

2018 ◽  
pp. 1-6
Author(s):  
A.H. Burstein ◽  
M. Sabbagh ◽  
R. Andrews ◽  
C. Valcarce ◽  
I. Dunn ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Small Molecule ◽  
Advanced Glycation Endproducts ◽  
Advanced Glycation ◽  
Phase 3 ◽  
Point Change ◽  
Glycation Endproducts ◽  
Orally Bioavailable

Increasing evidence supports the role of the Receptor for Advanced Glycation Endproducts (RAGE) in the pathology of Alzheimer’s disease. Azeliragon (TTP488) is an orally bioavailable small molecule inhibitor of RAGE in Phase 3 development as a potential treatment to slow disease progression in patients mild AD. Preclinical studies in animal models of AD (tgAPPSwedish/London) have shown azeliragon to decrease Aβ plaque deposition; reduce total Aβ brain concentration while increasing plasma Aβ levels; decreases sAPPβ while increasing sAPPα; reduce levels of inflammatory cytokines; and slow cognitive decline and improve cerebral blood flow. In the Phase 2b study, 18-months treatment in patients with mild-to-moderate AD indicated a baseline to endpoint change in ADAS-cog of 3.1 points in favor of drug. A greater magnitude of effect was evident in the sub-group of patients with mild AD (MMSE 21-26) with a baseline to endpoint change of 4 points on the ADAS-cog in favor of azeliragon and a 1 point change in CDR-sb in favor of drug. Azeliragon 5 mg/day delayed time to cognitive deterioration (7-point change in ADAS-cog from baseline, logrank p=0.0149). Based on promising results from the Phase 2b study, a Phase 3 registration program (STEADFAST) is being conducted under a Special Protocol Assessment from FDA. The ongoing Phase 3 program, if successful may demonstrate azeliragon can slow cognitive decline in mild AD patients.

scholarly journals Therapeutic Potential of Direct Clearance of the Amyloid-β in Alzheimer’s Disease

2020 ◽  
Vol 10 (2) ◽  
pp. 93 ◽  
Author(s):  
Dong Eun Kim ◽  
Ronny Priefer
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Therapeutic Potential ◽  
Advanced Glycation Endproducts ◽  
Amyloid Β ◽  
Solute Concentration ◽  
Advanced Glycation ◽  
Glycation Endproducts ◽  
The Brain ◽  
Lipoprotein Receptor Related Protein

Alzheimer’s disease (AD) is characterized by deposition and accumulation of amyloid-β (Aβ) and its corresponding plaques within the brain. Although much debate exists whether these plaques are the cause or the effect of AD, the accumulation of Aβ is linked with the imbalance between the production and clearance of Aβ. The receptor for advanced glycation endproducts (RAGE) facilitates entry of free Aβ from the peripheral stream. Conversely, lipoprotein receptor-related protein 1 (LRP1), located in the abluminal side at the blood–brain barrier mediates the efflux of Aβ. Research on altering the rates of clearance of Aβ by targeting these two pathways has been extensively study. Additionally, a cerebrospinal fluid (CSF) circulation assistant device has also been evaluated as an approach to increase solute concentration in the CSF via mechanical drainage, to allow for removal of Aβ from the brain. Herein, we provide a brief review of these approaches that are designed to re-establish a homeostatic Aβ balance in the brain.

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