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Amyloid-β42/40 ratio drives tau pathology in 3D human neural cell culture models of Alzheimer's disease

Nature communications, 2020-03, Vol.11 (1), p.1377-1377, Article 1377

2020

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STIM1, an essential and conserved component of store-operated Ca²⁺ channel function

The Journal of cell biology, 2005-05, Vol.169 (3), p.435-445

2005

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Genome-wide Association Analysis Reveals Putative Alzheimer's Disease Susceptibility Loci in Addition to APOE

American journal of human genetics, 2008-11, Vol.83 (5), p.623-632

2008

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The GSM BPN-15606 as a Potential Candidate for Preventative Therapy in Alzheimer's Disease

Journal of Alzheimer's disease, 2020-01, Vol.73 (4), p.1541

2020

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Transcriptomic profiling of sporadic Alzheimer's disease patients

Molecular brain, 2022-10, Vol.15 (1), p.83-83, Article 83

2022

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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

PloS one, 2015-02, Vol.10 (2), p.e0118379

2015

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Visualizing APP and BACE-1 approximation in neurons yields insight into the amyloidogenic pathway

Nature neuroscience, 2016-01, Vol.19 (1), p.55

2016

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

Nature (London), 2014-11, Vol.515 (7526), p.274-278

2014

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Cholesterol Metabolism Is a Druggable Axis that Independently Regulates Tau and Amyloid-β in iPSC-Derived Alzheimer’s Disease Neurons

Cell stem cell, 2019-03, Vol.24 (3), p.363-375.e9

2019

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And four equals one: Presenilin takes the γ-secretase role by itself

Proceedings of the National Academy of Sciences - PNAS, 2010-12, Vol.107 (50), p.21236-21237

2010

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Soluble Gamma-secretase Modulators Attenuate Alzheimer's β-amyloid Pathology and Induce Conformational Changes in Presenilin 1

EBioMedicine, 2017-10, Vol.24 (C), p.93-101

2017

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Preclinical validation of a potent γ-secretase modulator for Alzheimer's disease prevention

The Journal of experimental medicine, 2021-04, Vol.218 (4)

2021

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ATP Effects on Insulin-degrading Enzyme Are Mediated Primarily through Its Triphosphate Moiety

The Journal of biological chemistry, 2004-12, Vol.279 (52), p.54216-54220

2004

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Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase

Human molecular genetics, 2004-01, Vol.13 (2), p.159-170

2004

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Modulation of γ-Secretase Reduces β-Amyloid Deposition in a Transgenic Mouse Model of Alzheimer's Disease

Neuron (Cambridge, Mass.), 2010-09, Vol.67 (5), p.769-780

2010

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Effect of potent γ-secretase modulator in human neurons derived from multiple presenilin 1-induced pluripotent stem cell mutant carriers

JAMA neurology, 2014-12, Vol.71 (12), p.1481

2014

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Reduction of the expression of the late-onset Alzheimer’s disease (AD) risk-factor BIN1 does not affect amyloid pathology in an AD mouse model

The Journal of biological chemistry, 2019-03, Vol.294 (12), p.4477-4487

2019

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Potential late-onset Alzheimer's disease-associated mutations in the ADAM10 gene attenuate α-secretase activity

Human molecular genetics, 2009-10, Vol.18 (20), p.3987-3996

2009

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Molecular imaging of Alzheimer's disease-related gamma-secretase in mice and nonhuman primates

The Journal of experimental medicine, 2020-12, Vol.217 (12)

2020

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Pharmacological and Toxicological Properties of the Potent Oral γ -Secretase Modulator BPN-15606

The Journal of pharmacology and experimental therapeutics, 2017-07, Vol.362 (1), p.31

2017

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Endotype reversal as a novel strategy for screening drugs targeting familial Alzheimer's disease

Alzheimer's & dementia, 2022-11, Vol.18 (11), p.2117-2130

2022

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Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer’s disease

Proceedings of the National Academy of Sciences - PNAS, 2017-11, Vol.114 (45), p.E9665-E9674

2017

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Dedifferentiation and neuronal repression define familial Alzheimer's disease

Science advances, 2020-11, Vol.6 (46)

2020

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NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease

The Journal of clinical investigation, 2009-12, Vol.119 (12), p.3692-3702

2009

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γ-Secretase Partitioning into Lipid Bilayers Remodels Membrane Microdomains after Direct Insertion

Langmuir, 2020-06, Vol.36 (23), p.6569-6579

2020

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Amyloid-β42/40 ratio drives tau pathology in 3D human neural cell culture models of Alzheimer's disease

STIM1, an essential and conserved component of store-operated Ca²⁺ channel function

Genome-wide Association Analysis Reveals Putative Alzheimer's Disease Susceptibility Loci in Addition to APOE

The GSM BPN-15606 as a Potential Candidate for Preventative Therapy in Alzheimer's Disease

Transcriptomic profiling of sporadic Alzheimer's disease patients

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

Visualizing APP and BACE-1 approximation in neurons yields insight into the amyloidogenic pathway

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

Cholesterol Metabolism Is a Druggable Axis that Independently Regulates Tau and Amyloid-β in iPSC-Derived Alzheimer’s Disease Neurons

And four equals one: Presenilin takes the γ-secretase role by itself

Soluble Gamma-secretase Modulators Attenuate Alzheimer's β-amyloid Pathology and Induce Conformational Changes in Presenilin 1

Preclinical validation of a potent γ-secretase modulator for Alzheimer's disease prevention

ATP Effects on Insulin-degrading Enzyme Are Mediated Primarily through Its Triphosphate Moiety

Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase

Modulation of γ-Secretase Reduces β-Amyloid Deposition in a Transgenic Mouse Model of Alzheimer's Disease

Effect of potent γ-secretase modulator in human neurons derived from multiple presenilin 1-induced pluripotent stem cell mutant carriers

Reduction of the expression of the late-onset Alzheimer’s disease (AD) risk-factor BIN1 does not affect amyloid pathology in an AD mouse model

Potential late-onset Alzheimer's disease-associated mutations in the ADAM10 gene attenuate α-secretase activity

Molecular imaging of Alzheimer's disease-related gamma-secretase in mice and nonhuman primates

Pharmacological and Toxicological Properties of the Potent Oral γ -Secretase Modulator BPN-15606

Endotype reversal as a novel strategy for screening drugs targeting familial Alzheimer's disease

Lack of BACE1 S-palmitoylation reduces amyloid burden and mitigates memory deficits in transgenic mouse models of Alzheimer’s disease

Dedifferentiation and neuronal repression define familial Alzheimer's disease

NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease

γ-Secretase Partitioning into Lipid Bilayers Remodels Membrane Microdomains after Direct Insertion

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