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Co-Localization of Amyloid Beta and Tau Pathology in Alzheimer's Disease Synaptosomes

The American journal of pathology, 2008-06, Vol.172 (6), p.1683-1692

2008

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Pharmacological inhibition of nSMase2 reduces brain exosome release and α-synuclein pathology in a Parkinson's disease model

Molecular brain, 2021-04, Vol.14 (1), p.70-70, Article 70

2021

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Extensive p-Tau Pathology and SDS-Stable p-Tau Oligomers in Alzheimer's Cortical Synapses

Brain pathology (Zurich, Switzerland), 2012-11, Vol.22 (6), p.826-833

2012

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Correction to: Pharmacological inhibition of nSMase2 reduces brain exosome release and α-synuclein pathology in a Parkinson’s disease model

Molecular brain, 2021-07, Vol.14 (1), p.1-108, Article 108

2021

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Suppression of tau propagation using an inhibitor that targets the DK-switch of nSMase2

Biochemical and biophysical research communications, 2018-05, Vol.499 (4), p.751-757

2018

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Exosomal tau with seeding activity is released from Alzheimer's disease synapses, and seeding potential is associated with amyloid beta

Laboratory investigation, 2021-12, Vol.101 (12), p.1605-1617

2021

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Levels of Soluble Apolipoprotein E/Amyloid-β (Aβ) Complex Are Reduced and Oligomeric Aβ Increased with APOE4 and Alzheimer Disease in a Transgenic Mouse Model and Human Samples[S]

The Journal of biological chemistry, 2013-02, Vol.288 (8), p.5914-5926

2013

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Correction to: Pharmacological inhibition of nSMase2 reduces brain exosome release and [alpha]-synuclein pathology in a Parkinson's disease model

Molecular brain, 2021-07, Vol.14 (1)

2021

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Pharmacological inhibition of nSMase2 reduces brain exosome release and [alpha]-synuclein pathology in a Parkinson's disease model

Molecular brain, 2021-04, Vol.14 (1)

2021

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AD synapses contain abundant Aβ monomer and multiple soluble oligomers, including a 56-kDa assembly

Neurobiology of aging, 2012-08, Vol.33 (8), p.1545-1555

2012

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Synaptic changes in Alzheimer's disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence

The American journal of pathology, 2004-11, Vol.165 (5), p.1809-1817

2004

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Increased cholesterol in Aβ-positive nerve terminals from Alzheimer's disease cortex

Neurobiology of aging, 2007-01, Vol.28 (1), p.8-17

2007

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Apolipoprotein E level and cholesterol are associated with reduced synaptic amyloid beta in Alzheimer’s disease and apoE TR mouse cortex

Acta neuropathologica, 2012-01, Vol.123 (1), p.39-52

2012

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AD synapses contain abundant AI2 monomer and multiple soluble oligomers, including a 56-kDa assembly

Neurobiology of aging, 2012-08, Vol.33 (8), p.1545-1555

2012

Volltextzugriff (PDF)

Synaptic Changes in Alzheimer's Disease

The American journal of pathology, 2004-11, Vol.165 (5), p.1809-1817

2004

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Synaptic changes in Alzheimer's disease: Increased amyloid-β and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence. Commentary

The American journal of pathology, 2004, Vol.165 (5), p.1809-1464

2004

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Increased cholesterol in Abeta-positive nerve terminals from Alzheimer's disease cortex

Neurobiology of aging, 2007-01, Vol.28 (1), p.8-17

2007

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Pharmacology department. Antimicrobial resistance

The Journal of cardiovascular nursing, 1999-01, Vol.13 (2), p.66

Gylys, K H

1999

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Synaptic Changes in Alzheimer's Disease: Increased Amyloid-{beta} and Gliosis in Surviving Terminals Is Accompanied by Decreased PSD-95 Fluorescence

The American journal of pathology, 2004-11, Vol.165 (5), p.1809

2004

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Characterization of the Irreversible Inhibition of High‐Affinity Choline Transport Produced by Hemicholinium Mustard

Journal of neurochemistry, 1992-10, Vol.59 (4), p.1302-1308

1992

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Pharmacological characterization of novel inhibitors of high affinity choline transport

Gylys, Karen Hoppens

1993

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Co-Localization of Amyloid Beta and Tau Pathology in Alzheimer's Disease Synaptosomes

Pharmacological inhibition of nSMase2 reduces brain exosome release and α-synuclein pathology in a Parkinson's disease model

Extensive p-Tau Pathology and SDS-Stable p-Tau Oligomers in Alzheimer's Cortical Synapses

Correction to: Pharmacological inhibition of nSMase2 reduces brain exosome release and α-synuclein pathology in a Parkinson’s disease model

Suppression of tau propagation using an inhibitor that targets the DK-switch of nSMase2

Exosomal tau with seeding activity is released from Alzheimer's disease synapses, and seeding potential is associated with amyloid beta

Levels of Soluble Apolipoprotein E/Amyloid-β (Aβ) Complex Are Reduced and Oligomeric Aβ Increased with APOE4 and Alzheimer Disease in a Transgenic Mouse Model and Human Samples[S]

Correction to: Pharmacological inhibition of nSMase2 reduces brain exosome release and [alpha]-synuclein pathology in a Parkinson's disease model

Pharmacological inhibition of nSMase2 reduces brain exosome release and [alpha]-synuclein pathology in a Parkinson's disease model

AD synapses contain abundant Aβ monomer and multiple soluble oligomers, including a 56-kDa assembly

Synaptic changes in Alzheimer's disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence

Increased cholesterol in Aβ-positive nerve terminals from Alzheimer's disease cortex

Apolipoprotein E level and cholesterol are associated with reduced synaptic amyloid beta in Alzheimer’s disease and apoE TR mouse cortex

AD synapses contain abundant AI2 monomer and multiple soluble oligomers, including a 56-kDa assembly

Synaptic Changes in Alzheimer's Disease

Synaptic changes in Alzheimer's disease: Increased amyloid-β and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence. Commentary

Increased cholesterol in Abeta-positive nerve terminals from Alzheimer's disease cortex

Pharmacology department. Antimicrobial resistance

Synaptic Changes in Alzheimer's Disease: Increased Amyloid-{beta} and Gliosis in Surviving Terminals Is Accompanied by Decreased PSD-95 Fluorescence

Characterization of the Irreversible Inhibition of High‐Affinity Choline Transport Produced by Hemicholinium Mustard

Pharmacological characterization of novel inhibitors of high affinity choline transport

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