(Q48544171)

12 February 2018

title

Neurodegenerative disease: amyloid pores from pathogenic mutations. (English)

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12 February 2018

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1

Hilal A Lashuel

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12 February 2018

Dean Hartley

2

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12 February 2018

Benjamin M Petre

series ordinal

3

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12 February 2018

Thomas Walz

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4

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12 February 2018

Peter T Lansbury

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5

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12 February 2018

language of work or name

English

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publication date

1 July 2002

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12 February 2018

published in

Nature

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12 February 2018

volume

418

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12 February 2018

issue

6895

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12 February 2018

page(s)

291

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12 February 2018

https://scigraph.springernature.com/pub.10.1038/418291a

exact match

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cites work

Evolution of amyloid: what normal protein folding may tell us about fibrillogenesis and disease

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7 January 2021

Is there a cause-and-effect relationship between alpha-synuclein fibrillization and Parkinson's disease?

1 reference

7 January 2021

Protofibrillar intermediates of amyloid beta-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons.

1 reference

7 January 2021

Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins

1 reference

7 January 2021

Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo

1 reference

7 January 2021

The mechanism of islet amyloid polypeptide toxicity is membrane disruption by intermediate-sized toxic amyloid particles.

1 reference

7 January 2021

Deposition of transthyretin in early stages of familial amyloidotic polyneuropathy: evidence for toxicity of nonfibrillar aggregates

1 reference

7 January 2021

Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases

1 reference

7 January 2021

The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Abeta protofibril formation

1 reference

7 January 2021

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

1 reference

7 January 2021

Amyloid beta protein forms ion channels: implications for Alzheimer's disease pathophysiology

1 reference

7 January 2021

The channel hypothesis of Huntington's disease

1 reference

7 January 2021

Monomer-monomer interactions drive the prepore to pore conversion of a beta-barrel-forming cholesterol-dependent cytolysin

1 reference

7 January 2021

Identifiers

DOI

10.1038/418291A

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12 February 2018

Dimensions Publication ID

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12 February 2018