(Q53360220)

13 May 2018

title

Mixtures of wild-type and a pathogenic (E22G) form of Abeta40 in vitro accumulate protofibrils, including amyloid pores. (English)

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13 May 2018

1

Hilal A Lashuel

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13 May 2018

Dean M Hartley

2

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13 May 2018

Benjamin M Petre

3

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13 May 2018

Joseph S Wall

4

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13 May 2018

Martha N Simon

5

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13 May 2018

Thomas Walz

6

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13 May 2018

Peter T Lansbury

7

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13 May 2018

language of work or name

English

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publication date

1 September 2003

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13 May 2018

Journal of Molecular Biology

published in

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13 May 2018

volume

332

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13 May 2018

issue

4

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13 May 2018

page(s)

795-808

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13 May 2018

Alzheimer's disease: genotypes, phenotypes, and treatments

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7 January 2021

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7 January 2021

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7 January 2021

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Annular alpha-synuclein protofibrils are produced when spherical protofibrils are incubated in solution or bound to brain-derived membranes

7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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Charge states rather than propensity for beta-structure determine enhanced fibrillogenesis in wild-type Alzheimer's beta-amyloid peptide compared to E22Q Dutch mutant

7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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Acceleration of oligomerization, not fibrillization, is a shared property of both alpha-synuclein mutations linked to early-onset Parkinson's disease: implications for pathogenesis and therapy

7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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Non-fibrillar oligomeric species of the amyloid ABri peptide, implicated in familial British dementia, are more potent at inducing apoptotic cell death than protofibrils or mature fibrils

7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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Channel activity of deamidated isoforms of prion protein fragment 106-126 in planar lipid bilayers

7 January 2021

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Prion channel proteins and their role in vacuolation and neurodegenerative diseases

7 January 2021

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Vesicle permeabilization by protofibrillar alpha-synuclein is sensitive to Parkinson's disease-linked mutations and occurs by a pore-like mechanism.

7 January 2021

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Vesicle permeabilization by protofibrillar alpha-synuclein: implications for the pathogenesis and treatment of Parkinson's disease

7 January 2021

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The channel hypothesis of Alzheimer's disease: current status

7 January 2021

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Genetics of Parkinson's disease and biochemical studies of implicated gene products

7 January 2021

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Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders

7 January 2021

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7 January 2021

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10.1016/S0022-2836(03)00927-6

7 January 2021

Identifiers

DOI

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13 May 2018

release_wziuengjyfb4disoxebthkqi3q

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mapped directly with Wikidata item

24 November 2022

based on heuristic

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13 May 2018