Evidence For and Against a Pathogenic Role of Reduced γ-Secretase Activity in Familial Alzheimer's Disease. (Q38802911)

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1 April 2020

title

Evidence For and Against a Pathogenic Role of Reduced γ-Secretase Activity in Familial Alzheimer's Disease (English)

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4

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Morgan Newman

2

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Giuseppe Verdile

3

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Ian F. Musgrave

6

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Seyyed Hani Moussavi Nik

7

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Michael Lardelli

8

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author name string

Tanya Jayne

1

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Gerald Münch

5

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publication date

1 April 2016

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Journal of Alzheimer's Disease

1 April 2020

published in

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volume

52

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issue

3

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page(s)

781-799

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Creative Commons Attribution-NonCommercial 4.0 International

1 April 2020

copyright license

start time

23 May 2016

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April 2022 Public Data File from Crossref

copyright status

copyrighted

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Presenilins are not required for A beta 42 production in the early secretory pathway

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Photoactivated gamma-secretase inhibitors directed to the active site covalently label presenilin 1

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BACE1 and BACE2 enzymatic activities in Alzheimer's disease

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Cathepsin D displays in vitro beta-secretase-like specificity.

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Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE

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A GPCR/secretase complex regulates beta- and gamma-secretase specificity for Abeta production and contributes to AD pathogenesis.

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

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Phosphorylation of APP-CTF-AICD domains and interaction with adaptor proteins: signal transduction and/or transcriptional role--relevance for Alzheimer pathology

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The physiology of the β-amyloid precursor protein intracellular domain AICD.

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Proteases and proteolysis in Alzheimer disease: a multifactorial view on the disease process

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Equimolar production of amyloid beta-protein and amyloid precursor protein intracellular domain from beta-carboxyl-terminal fragment by gamma-secretase

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gamma-Secretase: successive tripeptide and tetrapeptide release from the transmembrane domain of beta-carboxyl terminal fragment

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When loss is gain: reduced presenilin proteolytic function leads to increased Abeta42/Abeta40. Talking Point on the role of presenilin mutations in Alzheimer disease

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The mechanism of γ-Secretase dysfunction in familial Alzheimer disease

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Visualization of A beta 42(43) and A beta 40 in senile plaques with end-specific A beta monoclonals: evidence that an initially deposited species is A beta 42(43).

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Presenilins and the gamma-secretase: still a complex problem

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Generation of Alzheimer disease-associated amyloid β42/43 peptide by γ-secretase can be inhibited directly by modulation of membrane thickness

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Qualitative changes in human γ-secretase underlie familial Alzheimer's disease

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Decreased clearance of CNS beta-amyloid in Alzheimer's disease

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

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Evidence That Levels of Presenilins (PS1 and PS2) Are Coordinately Regulated by Competition for Limiting Cellular Factors

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Three-amino acid spacing of presenilin endoproteolysis suggests a general stepwise cleavage of gamma-secretase-mediated intramembrane proteolysis

21 January 2018

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Familial frontotemporal dementia-associated presenilin-1 c.548G>T mutation causes decreased mRNA expression and reduced presenilin function in knock-in mice

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Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondria

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Oxidative protein folding in the endoplasmic reticulum: tight links to the mitochondria-associated membrane (MAM).

21 January 2018

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Upregulated function of mitochondria-associated ER membranes in Alzheimer disease

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Where the endoplasmic reticulum and the mitochondrion tie the knot: the mitochondria-associated membrane (MAM)

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Autophagosomes form at ER-mitochondria contact sites

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Alzheimer's disease-related misfolded proteins and dysfunctional organelles on autophagy menu.

21 January 2018

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21 January 2018

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APP intracellular domain derived from amyloidogenic β- and γ-secretase cleavage regulates neprilysin expression

21 January 2018

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The Aβ-clearance protein transthyretin, like neprilysin, is epigenetically regulated by the amyloid precursor protein intracellular domain.

21 January 2018

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Presenilins promote the cellular uptake of copper and zinc and maintain copper chaperone of SOD1-dependent copper/zinc superoxide dismutase activity

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Truncated and modified amyloid-beta species

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Resistance of human cerebrospinal fluid to in vitro oxidation is directly related to its amyloid-beta content

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Amyloid-beta and tau serve antioxidant functions in the aging and Alzheimer brain

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Abeta40, either soluble or aggregated, is a remarkably potent antioxidant in cell-free oxidative systems

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β-amyloid 1-42 induces physiological transcriptional regulation of BACE1.

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Nuclear translocation uncovers the amyloid peptide Aβ42 as a regulator of gene transcription.

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Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression

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

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β2-adrenoceptor activation modulates skin wound healing processes to reduce scarring

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Amyloid-β protein (Aβ) Glu11 is the major β-secretase site of β-site amyloid-β precursor protein-cleaving enzyme 1(BACE1), and shifting the cleavage site to Aβ Asp1 contributes to Alzheimer pathogenesis

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Nontranscriptional role of Hif-1α in activation of γ-secretase and notch signaling in breast cancer.

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Metabolome in progression to Alzheimer's disease

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Signaling pathways and mechanisms of hypoxia-induced autophagy in the animal cells

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21 January 2018

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Hypoxia-inducible factor 1alpha (HIF-1alpha)-mediated hypoxia increases BACE1 expression and beta-amyloid generation

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Mean age of onset in familial Alzheimer's disease is determined by amyloid beta 42.

21 January 2018

1 reference

Mean age-of-onset of familial alzheimer disease caused by presenilin mutations correlates with both increased Abeta42 and decreased Abeta40.

21 January 2018

1 reference

Alzheimer's Aβ(1–42) is generated in the endoplasmic reticulum/intermediate compartment of NT2N cells

21 January 2018

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Distinct sites of intracellular production for Alzheimer's disease A beta40/42 amyloid peptides.

21 January 2018

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A Novel γ-Secretase Assay Based on Detection of the Putative C-terminal Fragment-γ of Amyloid β Protein Precursor

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21 January 2018

Identifiers

DOI

10.3233/JAD-151186

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:27060961 AND SRC:MED&resulttype=core&format=json

1 April 2020

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