scispace - formally typeset
Journal ArticleDOI

Molecular mechanisms of amyloidosis.

Giampaolo Merlini, +1 more
- 07 Aug 2003 - 
- Vol. 349, Iss: 6, pp 583-596
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
More filters
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

Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness: A Scientific Statement From the American Heart Association

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
More filters
Journal ArticleDOI

The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

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.

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

Diffusible, nonfibrillar ligands derived from Aβ1–42 are potent central nervous system neurotoxins

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.

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.
Related Papers (5)