Journal ArticleDOI
Molecular mechanisms of amyloidosis.
TLDR
The molecular basis of various types of amyloidosis is reviewed and new ways of treating these disorders are proposed.Abstract:
Amyloidosis affects millions of people, as a cause of Alzheimer's disease or a complication of dialysis, and also causes rare conditions. The many forms of the disorder have one underlying principle: misfolded proteins. Prompt, correct diagnosis is essential, especially in the inherited forms of amyloidosis. This article reviews the molecular basis of various types of amyloidosis and proposes new ways of treating these disorders.read more
Citations
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Journal ArticleDOI
Protein Misfolding, Functional Amyloid, and Human Disease
TL;DR: The relative importance of the common main-chain and side-chain interactions in determining the propensities of proteins to aggregate is discussed and some of the evidence that the oligomeric fibril precursors are the primary origins of pathological behavior is described.
Journal ArticleDOI
Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease
Randall J. Bateman,Chengjie Xiong,Tammie L.S. Benzinger,Anne M. Fagan,Alison Goate,Nick C. Fox,Daniel S. Marcus,Nigel J. Cairns,Xianyun Xie,Tyler Blazey,David M. Holtzman,Anna Santacruz,Virginia Buckles,Angela Oliver,Krista L. Moulder,Paul S. Aisen,Bernardino Ghetti,William E. Klunk,Eric McDade,Ralph N. Martins,Colin L. Masters,Richard Mayeux,John M. Ringman,Martin N. Rossor,Peter R. Schofield,Reisa A. Sperling,Stephen Salloway,John C. Morris +27 more
TL;DR: In this paper, a longitudinal study of 128 patients with Alzheimer's disease was conducted, where the authors used the participant's age at baseline assessment and the parent's age to calculate the estimated years from expected symptom onset (age of the participant minus parent's ages at symptom onset).
Journal ArticleDOI
Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness: A Scientific Statement From the American Heart Association
Raymond R. Townsend,Ian B. Wilkinson,Ernesto L. Schiffrin,Alberto Avolio,Julio A. Chirinos,John R. Cockcroft,Kevin S. Heffernan,Edward G. Lakatta,Carmel M. McEniery,Gary F. Mitchell,Samer S. Najjar,Wilmer W. Nichols,Elaine M. Urbina,Thomas Weber +13 more
TL;DR: The field of arterial stiffness investigation, which has exploded over the past 20 years, has proliferated without logistical guidance for clinical and research studies, and questions that remain to be addressed in this field are addressed.
Journal ArticleDOI
Conformational constraints for amyloid fibrillation: the importance of being unfolded.
TL;DR: In this review, recent findings are surveyed to illustrate that protein fibrillogenesis requires a partially folded conformation, which is relatively unfolded, and shares many structural properties with the pre-molten globule state.
Journal ArticleDOI
Neurodegenerative diseases and oxidative stress.
TL;DR: The role of mitochondria in apoptosis is crucial as discussed by the authors and its role is pivotal for modulation of critical cellular functions, notably for neurons astrocytes and microglia, such as apoptosis program activation, and ion transport, calcium mobilization, involved in excitotoxicity.
References
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Journal ArticleDOI
The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
John Hardy,Dennis J. Selkoe +1 more
TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.
Journal ArticleDOI
Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo.
Dominic M. Walsh,Igor Klyubin,Julia V. Fadeeva,William K. Cullen,Roger Anwyl,Michael S. Wolfe,Michael J. Rowan,Dennis J. Selkoe +7 more
TL;DR: It is reported that natural oligomers of human Aβ are formed soon after generation of the peptide within specific intracellular vesicles and are subsequently secreted from the cell, indicating that synaptotoxic Aβ oligomers can be targeted therapeutically.
Journal ArticleDOI
Effects of Age, Sex, and Ethnicity on the Association Between Apolipoprotein E Genotype and Alzheimer Disease: A Meta-analysis
Lindsay A. Farrer,L. Adrienne Cupples,Jonathan L. Haines,Bradley T. Hyman,Walter A. Kukull,Richard Mayeux,Richard H. Myers,Margaret A. Pericak-Vance,Neil Risch,Cornelia M. van Duijn +9 more
TL;DR: The APOE∈4 allele represents a major risk factor for AD in all ethnic groups studied, across all ages between 40 and 90 years, and in both men and women.
Journal ArticleDOI
Diffusible, nonfibrillar ligands derived from Aβ1–42 are potent central nervous system neurotoxins
Mary P. Lambert,A. K. Barlow,Brett A. Chromy,C. Edwards,R. Freed,M. Liosatos,Todd E. Morgan,Irina Rozovsky,Barbara L. Trommer,Kirsten L. Viola,Pat Wals,Chuan Zhang,Caleb E. Finch,Grant A. Krafft,William L. Klein +14 more
TL;DR: It is hypothesized that impaired synaptic plasticity and associated memory dysfunction during early stage Alzheimer's disease and severe cellular degeneration and dementia during end stage could be caused by the biphasic impact of Abeta-derived diffusible ligands acting upon particular neural signal transduction pathways.
Journal ArticleDOI
Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.
Dale Schenk,Robin Barbour,Whitney Dunn,Grace Gordon,Henry Grajeda,Teresa Guido,Kang Hu,Jiping Huang,Kelly Johnson-Wood,Karen Khan,Dora Kholodenko,Michael K. Lee,Zhenmei Liao,Ivan Lieberburg,Ruth Motter,Linda Mutter,Ferdie Soriano,George Shopp,Vasquez Nicki J,Christopher Vandevert,Shannan Walker,Mark Wogulis,Ted Yednock,Dora Games,Peter Seubert +24 more
TL;DR: It is reported that immunization of the young animals essentially prevented the development of β-amyloid-plaque formation, neuritic dystrophy and astrogliosis, and treatment of the older animals markedly reduced the extent and progression of these AD-like neuropathologies.
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