The amyloid cascade and Alzheimer's disease therapeutics: theory versus observation DOI Creative Commons

Rudy J. Castellani,

Germán Plascencia‐Villa, George Perry

et al.

Laboratory Investigation, Journal Year: 2019, Volume and Issue: 99(7), P. 958 - 970

Published: Feb. 13, 2019

Language: Английский

A new era for understanding amyloid structures and disease DOI
M.G. Iadanza, Matthew P. Jackson, Eric W. Hewitt

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2018, Volume and Issue: 19(12), P. 755 - 773

Published: Sept. 20, 2018

Language: Английский

Citations

869

Structural variation in amyloid-β fibrils from Alzheimer's disease clinical subtypes DOI
Wei Qiang,

Wai‐Ming Yau,

Junxia Lu

et al.

Nature, Journal Year: 2017, Volume and Issue: 541(7636), P. 217 - 221

Published: Jan. 1, 2017

Language: Английский

Citations

581

Amyloid Oligomers: A Joint Experimental/Computational Perspective on Alzheimer’s Disease, Parkinson’s Disease, Type II Diabetes, and Amyotrophic Lateral Sclerosis DOI
Phuong H. Nguyen, Ayyalusamy Ramamoorthy, Bikash R. Sahoo

et al.

Chemical Reviews, Journal Year: 2021, Volume and Issue: 121(4), P. 2545 - 2647

Published: Feb. 5, 2021

Protein misfolding and aggregation is observed in many amyloidogenic diseases affecting either the central nervous system or a variety of peripheral tissues. Structural dynamic characterization all species along pathways from monomers to fibrils challenging by experimental computational means because they involve intrinsically disordered proteins most diseases. Yet understanding how amyloid become toxic challenge developing treatment for these Here we review what computer, vitro, vivo, pharmacological experiments tell us about accumulation deposition oligomers (Aβ, tau), α-synuclein, IAPP, superoxide dismutase 1 proteins, which have been mainstream concept underlying Alzheimer's disease (AD), Parkinson's (PD), type II diabetes (T2D), amyotrophic lateral sclerosis (ALS) research, respectively, years.

Language: Английский

Citations

552

Half a century of amyloids: past, present and future DOI Creative Commons
Pu Chun Ke, Ruhong Zhou, Louise C. Serpell

et al.

Chemical Society Reviews, Journal Year: 2020, Volume and Issue: 49(15), P. 5473 - 5509

Published: Jan. 1, 2020

Amyloid diseases are global epidemics with profound health, social and economic implications yet remain without a cure. This dire situation calls for research into the origin pathological manifestations of amyloidosis to stimulate continued development new therapeutics. In basic science engineering, cross-β architecture has been constant thread underlying structural characteristics functional amyloids, realizing that amyloid structures can be both in nature fuelled innovations artificial whose use today ranges from water purification 3D printing. At conclusion half century since Eanes Glenner's seminal study amyloids humans, this review commemorates occasion by documenting major milestones date, perspectives biology, biophysics, medicine, microbiology, engineering nanotechnology. We also discuss challenges opportunities drive interdisciplinary field moving forward.

Language: Английский

Citations

486

The preclinical phase of the pathological process underlying sporadic Alzheimer’s disease DOI Open Access
Heiko Braak, Kelly Del Tredici

Brain, Journal Year: 2015, Volume and Issue: 138(10), P. 2814 - 2833

Published: Aug. 17, 2015

Abnormal tau lesions (non-argyrophilic pretangle material, argyrophilic neuropil threads, neurofibrillary tangles) in select types of neurons are crucial for the pathogenesis sporadic Alzheimer's disease. Ongoing formation these persists into end-stage disease and is not subject to remission. The early phase a focus increasing interest because only abnormal forms microtubule-associated protein involved at that point and, contrast late-stage when amyloid-β deposition present, this temporally closer prevailing conditions induce pathological process underlying Extracellular aggregated may be produced under by nerve cells contain tau. One potential trigger hyperphosphorylation conformational change presence non-endogenous pathogen. Subsequently, predictable regional distribution pattern develops phylogenetically late-appearing ontogenetically late-maturing connected via their axons. It hoped hypotheses drawn from considerations, as well recent dissemination models, studies variant conformers, imaging will encourage development new preventative disease-modifying strategies.

Language: Английский

Citations

467

Propagation and spread of pathogenic protein assemblies in neurodegenerative diseases DOI
Mathias Jucker, Lary C. Walker

Nature Neuroscience, Journal Year: 2018, Volume and Issue: 21(10), P. 1341 - 1349

Published: Sept. 20, 2018

Language: Английский

Citations

367

Amyloid-β and tau complexity — towards improved biomarkers and targeted therapies DOI
Juan Carlos Polanco, Chuanzhou Li, Liviu‐Gabriel Bodea

et al.

Nature Reviews Neurology, Journal Year: 2017, Volume and Issue: 14(1), P. 22 - 39

Published: Dec. 15, 2017

Language: Английский

Citations

351

A clinicopathological approach to the diagnosis of dementia DOI
Fanny M. Elahi, Bruce L. Miller

Nature Reviews Neurology, Journal Year: 2017, Volume and Issue: 13(8), P. 457 - 476

Published: July 14, 2017

Language: Английский

Citations

334

Mammalian prions and their wider relevance in neurodegenerative diseases DOI
John Collinge

Nature, Journal Year: 2016, Volume and Issue: 539(7628), P. 217 - 226

Published: Nov. 1, 2016

Language: Английский

Citations

231

The complexity of Alzheimer’s disease: an evolving puzzle DOI
Camilla Ferrari, Sandro Sorbi

Physiological Reviews, Journal Year: 2021, Volume and Issue: 101(3), P. 1047 - 1081

Published: Jan. 21, 2021

The history of Alzheimer's disease (AD) started in 1907, but we needed to wait until the end century identify components pathological hallmarks and genetic subtypes formulate first pathogenic hypothesis. Thanks biomarkers new technologies, concept AD then rapidly changed from a static view an amnestic dementia presenium biological entity that could be clinically manifested as normal cognition or different types. What is clearly emerging studies heterogeneous each aspect, such amyloid composition, tau distribution, relation between tau, clinical symptoms, background, thus it probably impossible explain with single process. scientific approach suffers chronological mismatches clinical, pathological, technological data, causing difficulty conceiving diagnostic gold standards creating models for drug discovery screening. A recent mathematical computer-based offers opportunity study real life provide point final missing pieces puzzle.

Language: Английский

Citations

214