scholarly journals Elucidating the Structures of Amyloid Oligomers with Macrocyclic β-Hairpin Peptides: Insights into Alzheimer’s Disease and Other Amyloid Diseases

2018 ◽  
Vol 51 (3) ◽  
pp. 706-718 ◽  
Author(s):  
Adam G. Kreutzer ◽  
James S. Nowick
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Oligomers ◽  
Hairpin Peptides ◽  
Amyloid Diseases

Does protein aggregation drive postmitotic tissue degeneration?

2021 ◽  
Vol 13 (577) ◽  
pp. eaax0914 ◽  
Author(s):  
Jeffery W. Kelly
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Protein Aggregation ◽  
Protein Aggregate ◽  
Tissue Degeneration ◽  
Disease Modifying Therapies ◽  
Disease Modifying ◽  
Amyloid Diseases ◽  
Aggregate Structures

Pharmacological evidence, from clinical trials where patients with systemic amyloid diseases are treated with disease-modifying therapies, supports the notion that protein aggregation drives tissue degeneration in these disorders. The protein aggregate structures driving tissue pathology and the commonalities in etiology between these diseases and Alzheimer’s disease are under investigation.

P2-392: The efficacy of anti-beta-amyloid oligomers antibody in mouse models of Alzheimer's disease

2013 ◽  
Vol 9 ◽  
pp. P502-P502
Author(s):  
Yasuhide Okamoto ◽  
Tatsuki Yokoseki ◽  
Takamatsu Naofumi ◽  
Yukiho Imai ◽  
Shinobu Fujii
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Models ◽  
Beta Amyloid ◽  
Amyloid Oligomers

scholarly journals Amyloid and Alzheimer's Disease: Inside and Out

2012 ◽  
Vol 39 (3) ◽  
pp. 286-298 ◽  
Author(s):  
Joshua H. K. Tam ◽  
Stephen H. Pasternak
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Clinical Implications ◽  
Amyloid Cascade Hypothesis ◽  
Amyloid Peptides ◽  
Amyloid Hypothesis ◽  
Lysosomal Dysfunction ◽  
Amyloid Oligomers ◽  
Amyloid Cascade

Alzheimer's disease (AD) is poised to become the most serious healthcare issue of our generation. The leading theory of AD pathophysiology is the Amyloid Cascade Hypothesis, and clinical trials are now proceeding based on this hypothesis. Here, we review the original evidence for the Amyloid Hypothesis, which was originally focused on the extracellular deposition of beta amyloid peptides (Aβ) in large fibrillar aggregates, as well as how this theory has been extended in recent years to focus on highly toxic small soluble amyloid oligomers. We will also examine emerging evidence that Aβ may actually begin to accumulate intracellularly in lysosomes, and the role for intracellular Aβ and lysosomal dysfunction may play in AD pathophysiology. Finally, we will review the clinical implications of these findings.

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