Log in to save to my catalogue

Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer's Disease and Do...

Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer's Disease and Do...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_jstor_primary_25665204

Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer's Disease and Down syndrome

About this item

Full title

Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer's Disease and Down syndrome

Publisher

United States: National Academy of Sciences

Journal title

Proceedings of the National Academy of Sciences - PNAS, 2010-04, Vol.107 (14), p.6538-6543

Language

English

Formats

Publication information

Publisher

United States: National Academy of Sciences

More information

Scope and Contents

Contents

Full-length amyloid beta peptides (Aβ₁₋₄₀/₄₂) form neuritic amyloid plaques in Alzheimer's disease (AD) patients and are implicated in AD pathology. However, recent transgenic animal models cast doubt on their direct role in AD pathology. Nonamyloidogenic truncated amyloid-beta fragments (Aβ₁₁₋₄₂ and Aβ₁₇₋₄₂) are also found in amyloid plaques of AD...

Alternative Titles

Full title

Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer's Disease and Down syndrome

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_jstor_primary_25665204

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_jstor_primary_25665204

Other Identifiers

ISSN

0027-8424,1091-6490

E-ISSN

1091-6490

DOI

10.1073/pnas.0914251107

How to access this item