A γ-secretase inhibitor, but not a γ-secretase modulator, induced defects in BDNF axonal trafficking and signaling: evidence for a role for APP (Q27314017)

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English	A γ-secretase inhibitor, but not a γ-secretase modulator, induced defects in BDNF axonal trafficking and signaling: evidence for a role for APP	scientific article

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A γ-secretase inhibitor, but not a γ-secretase modulator, induced defects in BDNF axonal trafficking and signaling: evidence for a role for APP (English)

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Rudolph E. Tanzi

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Rudolph E Tanzi

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author name string

April M Weissmiller

1

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Orlangie Natera-Naranjo

2

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Sol M Reyna

3

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Matthew L Pearn

4

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Xiaobei Zhao

5

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Phuong Nguyen

6

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Soan Cheng

7

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Lawrence S B Goldstein

8

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Steven L Wagner

10

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William C Mobley

11

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Chengbiao Wu

12

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language of work or name

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publication date

2015

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10

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e0118379

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Creative Commons Attribution 4.0 International

24 February 2015

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April 2022 Public Data File from Crossref

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Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC4339551/fullTextXML

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Potential use of γ-secretase modulators in the treatment of Alzheimer disease

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APP regulates NGF receptor trafficking and NGF-mediated neuronal differentiation and survival

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Early BDNF treatment ameliorates cell loss in the entorhinal cortex of APP transgenic mice

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BDNF-based synaptic repair as a disease-modifying strategy for neurodegenerative diseases

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Development and mechanism of γ-secretase modulators for Alzheimer's disease

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γ-secretase modulators and presenilin 1 mutants act differently on presenilin/γ-secretase function to cleave Aβ42 and Aβ43.

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Current advances in using neurotrophic factors to treat neurodegenerative disorders

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28 September 2017

The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus

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Alzheimer disease in 2020.

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Safety and tolerability of the γ-secretase inhibitor avagacestat in a phase 2 study of mild to moderate Alzheimer disease

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Enhanced β-secretase processing alters APP axonal transport and leads to axonal defects

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Snapin recruits dynein to BDNF-TrkB signaling endosomes for retrograde axonal transport and is essential for dendrite growth of cortical neurons

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Functional characterization and axonal transport of quantum dot labeled BDNF.

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γ-Secretase modulator in Alzheimer's disease: shifting the end.

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Inhibition of γ-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia

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First and second generation γ-secretase modulators (GSMs) modulate amyloid-β (Aβ) peptide production through different mechanisms

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Differential effects between γ-secretase inhibitors and modulators on cognitive function in amyloid precursor protein-transgenic and nontransgenic mice

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β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia

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γ-Secretase inhibitors and modulators for Alzheimer's disease

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Amyloid-β annular protofibrils evade fibrillar fate in Alzheimer disease brain

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Amyloid beta dimers/trimers potently induce cofilin-actin rods that are inhibited by maintaining cofilin-phosphorylation

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Amyloid beta impairs mitochondrial anterograde transport and degenerates synapses in Alzheimer's disease neurons

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γ-Secretase Modulators as Potential Disease Modifying Anti-Alzheimer’s Drugs

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Modulation of gamma-secretase reduces beta-amyloid deposition in a transgenic mouse model of Alzheimer's disease

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Aβ oligomers inhibit synapse remodelling necessary for memory consolidation

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Alzheimer's-related endosome dysfunction in Down syndrome is Abeta-independent but requires APP and is reversed by BACE-1 inhibition.

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Proteolytic processing of the Alzheimer disease-associated presenilin-1 generates an in vivo substrate for protein kinase C.

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28 September 2017

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The beta-amyloid protein precursor of Alzheimer disease has soluble derivatives found in human brain and cerebrospinal fluid

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Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport

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28 September 2017

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Brain transplants of cells expressing the carboxyl-terminal fragment of the Alzheimer amyloid protein precursor cause specific neuropathology in vivo

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31 May 2018

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31 May 2018

Altered protein composition of isolated human cortical neurons in Alzheimer disease

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Overexpression of amyloid precursor protein alters its normal processing and is associated with neurotoxicity

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31 May 2018

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31 May 2018

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31 May 2018

Neuroscience: Alzheimer's disease

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21 January 2018

A phase 3 trial of semagacestat for treatment of Alzheimer's disease

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The origins of Alzheimer disease: a is for amyloid.

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21 January 2018

Distinct early folding and aggregation properties of Alzheimer amyloid-beta peptides Abeta40 and Abeta42: stable trimer or tetramer formation by Abeta42.

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21 January 2018

The influence of the carboxyl terminus of the Alzheimer Abeta peptide on its conformation, aggregation, and neurotoxic properties

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21 January 2018

Gamma-secretase: proteasome of the membrane?

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21 January 2018

BMS-708,163 targets presenilin and lacks notch-sparing activity

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21 January 2018

A subset of NSAIDs lower amyloidogenic Abeta42 independently of cyclooxygenase activity

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Recombinant BDNF rescues deficits in basal synaptic transmission and hippocampal LTP in BDNF knockout mice.

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Reductions in beta-amyloid concentrations in vivo by the gamma-secretase inhibitors BMS-289948 and BMS-299897.

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Gamma-secretase inhibitors: Notch so bad.

1 reference

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0118379

21 January 2018

Gamma-secretase inhibition reduces spine density in vivo via an amyloid precursor protein-dependent pathway.

1 reference

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0118379

21 January 2018

Impaired learning and LTP in mice expressing the carboxy terminus of the Alzheimer amyloid precursor protein

1 reference

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0118379

21 January 2018

Dynein motors transport activated Trks to promote survival of target-dependent neurons

1 reference

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0118379

21 January 2018

Disruption of axonal transport and neuronal viability by amyloid precursor protein mutations in Drosophila.

1 reference

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0118379

21 January 2018

Neuronal overexpression of APPL, the Drosophila homologue of the amyloid precursor protein (APP), disrupts axonal transport.

1 reference

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0118379

21 January 2018

Acute impairment of mitochondrial trafficking by beta-amyloid peptides in hippocampal neurons.

1 reference

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0118379

21 January 2018

Trophic factors: 50 years of growth

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4339551

28 November 2018

Memory impairment and cholinergic dysfunction by centrally administered Abeta and carboxyl-terminal fragment of Alzheimer's APP in mice

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=4339551

28 November 2018

Presenilin-1 regulates intracellular trafficking and cell surface delivery of beta-amyloid precursor protein

1 reference

https://pubmed.ncbi.nlm.nih.gov/25710492

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Identifiers

10.1371/JOURNAL.PONE.0118379

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

2015PLoSO..1018379W

0 references

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

PMC publication ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

PubMed publication ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

ResearchGate publication ID

0 references

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