(Q27314017)

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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

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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

9

object named as

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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2

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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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inferred from PubMed Central ID database lookup

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

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Real-time imaging of axonal transport of quantum dot-labeled BDNF in primary neurons

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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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Defective axonal transport of Rab7 GTPase results in dysregulated trophic signaling.

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

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28 September 2017

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

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28 September 2017

Modulation of γ-secretase by EVP-0015962 reduces amyloid deposition and behavioral deficits in Tg2576 mice

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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

1 reference

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

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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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28 September 2017

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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28 September 2017

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

1 reference

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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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Deciphering Alzheimer disease

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28 September 2017

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

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Amyloid precursor protein revisited: neuron-specific expression and highly stable nature of soluble derivatives.

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γ-Secretase inhibitors and modulators for Alzheimer's disease

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Dissociation between the processivity and total activity of γ-secretase: implications for the mechanism of Alzheimer's disease-causing presenilin mutations

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

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The many substrates of presenilin/γ-secretase

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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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Amyloid Beta Annular Protofibrils in Cell Processes and Synapses Accumulate with Aging and Alzheimer-Associated Genetic Modification

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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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β-Amyloid impairs axonal BDNF retrograde trafficking

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Axonal transport of mitochondria requires milton to recruit kinesin heavy chain and is light chain independent

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Amyloid precursor protein and Notch intracellular domains are generated after transport of their precursors to the cell surface

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28 September 2017

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28 September 2017

Notch and Presenilin: regulated intramembrane proteolysis links development and degeneration.

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28 September 2017

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28 September 2017

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28 September 2017

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

Excessive production of amyloid beta-protein by peripheral cells of symptomatic and presymptomatic patients carrying the Swedish familial Alzheimer disease mutation

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28 September 2017

Beta-amyloid precursor protein of Alzheimer disease occurs as 110- to 135-kilodalton membrane-associated proteins in neural and nonneural tissues.

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28 September 2017

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

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28 September 2017

Neurotoxicity of a fragment of the amyloid precursor associated with Alzheimer's disease

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28 September 2017

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

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28 September 2017

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28 September 2017

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

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28 September 2017

Deposition of beta/A4 immunoreactivity and neuronal pathology in transgenic mice expressing the carboxyl-terminal fragment of the Alzheimer amyloid precursor in the brain

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28 September 2017

A three-dimensional human neural cell culture model of Alzheimer's disease

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31 May 2018

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31 May 2018

Soluble Aβ oligomers inhibit long-term potentiation through a mechanism involving excessive activation of extrasynaptic NR2B-containing NMDA receptors

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31 May 2018

Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease

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31 May 2018

An etiological role of amyloidogenic carboxyl-terminal fragments of the beta-amyloid precursor protein in Alzheimer's disease.

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31 May 2018

Altered protein composition of isolated human cortical neurons in Alzheimer disease

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31 May 2018

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

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31 May 2018

Brain-derived neurotrophic factor prevents the death of motoneurons in newborn rats after nerve section

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31 May 2018

Degeneration in vitro of post-mitotic neurons overexpressing the Alzheimer amyloid protein precursor.

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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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21 January 2018

The origins of Alzheimer disease: a is for amyloid.

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21 January 2018

A seed for Alzheimer amyloid in the brain.

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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

Temporal profile of amyloid-beta (Abeta) oligomerization in an in vivo model of Alzheimer disease. A link between Abeta and tau pathology

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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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21 January 2018

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

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21 January 2018

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

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21 January 2018

Gamma-secretase inhibitors: Notch so bad.

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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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