Generation and deposition of Aβ43 by the virtually inactive presenilin-1 L435F mutant contradicts the presenilin loss-of-function hypothesis of Alzheimer's disease (Q41772002)

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scientific article published on 17 March 2016

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English	Generation and deposition of Aβ43 by the virtually inactive presenilin-1 L435F mutant contradicts the presenilin loss-of-function hypothesis of Alzheimer's disease	scientific article published on 17 March 2016

Statements

scholarly article

1 reference

Europe PubMed Central

9 October 2017

Generation and deposition of Aβ43 by the virtually inactive presenilin-1 L435F mutant contradicts the presenilin loss-of-function hypothesis of Alzheimer's disease (English)

1 reference

Europe PubMed Central

9 October 2017

Alzheimer's disease

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Peer-Hendrik Kuhn

5

1 reference

Europe PubMed Central

9 October 2017

Christian Haass

9

object named as

Christian Haass

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Stefan F Lichtenthaler

8

object named as

Stefan F Lichtenthaler

1 reference

Europe PubMed Central

9 October 2017

Thomas Arzberger

10

object named as

Thomas Arzberger

1 reference

Europe PubMed Central

9 October 2017

author name string

Benedikt Kretner

1

1 reference

Europe PubMed Central

9 October 2017

Johannes Trambauer

2

1 reference

Europe PubMed Central

9 October 2017

Akio Fukumori

3

1 reference

Europe PubMed Central

9 October 2017

Janina Mielke

4

1 reference

Europe PubMed Central

9 October 2017

Elisabeth Kremmer

6

1 reference

Europe PubMed Central

9 October 2017

Armin Giese

7

1 reference

Europe PubMed Central

9 October 2017

Harald Steiner

11

1 reference

Europe PubMed Central

9 October 2017

publication date

17 March 2016

1 reference

Europe PubMed Central

9 October 2017

EMBO Molecular Medicine

1 reference

Europe PubMed Central

9 October 2017

8

1 reference

Europe PubMed Central

9 October 2017

458-465

1 reference

Europe PubMed Central

9 October 2017

5

1 reference

Europe PubMed Central

9 October 2017

Aβ43 is neurotoxic and primes aggregation of Aβ40 in vivo

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Presenilin-1 knockin mice reveal loss-of-function mechanism for familial Alzheimer's disease

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Carnosic acid attenuates apoptosis induced by amyloid-β 1-42 or 1-43 in SH-SY5Y human neuroblastoma cells.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Trans-dominant negative effects of pathogenic PSEN1 mutations on γ-secretase activity and Aβ production.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

The mechanism of γ-Secretase dysfunction in familial Alzheimer disease

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Molecular consequences of amyloid precursor protein and presenilin mutations causing autosomal-dominant Alzheimer's disease

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Potent amyloidogenicity and pathogenicity of Aβ43.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Regulated intramembrane proteolysis--lessons from amyloid precursor protein processing

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Neurotoxicity of Alzheimer's disease Aβ peptides is induced by small changes in the Aβ42 to Aβ40 ratio

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

ADAM10 is the physiologically relevant, constitutive alpha-secretase of the amyloid precursor protein in primary neurons

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

A presenilin-1 mutation identified in familial Alzheimer disease with cotton wool plaques causes a nearly complete loss of gamma-secretase activity

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Generation of Abeta38 and Abeta42 is independently and differentially affected by familial Alzheimer disease-associated presenilin mutations and gamma-secretase modulation

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Pathological activity of familial Alzheimer's disease-associated mutant presenilin can be executed by six different gamma-secretase complexes

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Random mutagenesis of presenilin-1 identifies novel mutants exclusively generating long amyloid beta-peptides.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Presenilin-1 mutations of leucine 166 equally affect the generation of the Notch and APP intracellular domains independent of their effect on Abeta 42 production

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Presenilin-dependent gamma-secretase processing of beta-amyloid precursor protein at a site corresponding to the S3 cleavage of Notch

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Glycine 384 is required for presenilin-1 function and is conserved in bacterial polytopic aspartyl proteases

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

The biological and pathological function of the presenilin-1 Deltaexon 9 mutation is independent of its defect to undergo proteolytic processing

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Cellular expression and proteolytic processing of presenilin proteins is developmentally regulated during neuronal differentiation.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increases beta-protein production

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

6 June 2018

Aβ43 is the earliest-depositing Aβ species in APP transgenic mouse brain and is converted to Aβ41 by two active domains of ACE.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

Important functional role of residue x of the presenilin GxGD protease active site motif for APP substrate cleavage specificity and substrate selectivity of γ-secretase.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

Gamma-secretase gene mutations in familial acne inversa

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

Abeta43 is more frequent than Abeta40 in amyloid plaque cores from Alzheimer disease brains.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

The GxGD motif of presenilin contributes to catalytic function and substrate identification of gamma-secretase.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

A presenilin 1 R278I mutation presenting with language impairment.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

Reconstitution of gamma-secretase activity

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

Abeta deposition is associated with neuropil changes, but not with overt neuronal loss in the human amyloid precursor protein V717F (PDAPP) transgenic mouse.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

Improved electrophoretic separation and immunoblotting of beta-amyloid (A beta) peptides 1-40, 1-42, and 1-43.

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5119496

18 August 2018

Amyloid beta-protein ending at Thr43 is a minor component of some diffuse plaques in the Alzheimer's disease brain, but is not found in cerebrovascular amyloid

1 reference

https://pubmed.ncbi.nlm.nih.gov/26988102

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Correlation between Abetax-40-, Abetax-42-, and Abetax-43-containing amyloid plaques and cognitive decline

1 reference

https://pubmed.ncbi.nlm.nih.gov/26988102

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Identifiers

10.15252/EMMM.201505952

1 reference

Europe PubMed Central

9 October 2017

1 reference

Europe PubMed Central

9 October 2017

1 reference

Europe PubMed Central

9 October 2017

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0 references

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