(Q34071519)

30 July 2017

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title

Modeling Alzheimer's disease in transgenic mice: effect of age and of presenilin1 on amyloid biochemistry and pathology in APP/London mice (English)

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30 July 2017

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Dewachter I

1

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30 July 2017

van Dorpe J

2

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30 July 2017

Spittaels K

3

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30 July 2017

Tesseur I

4

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30 July 2017

Van Den Haute C

5

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30 July 2017

Moechars D

6

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30 July 2017

Van Leuven F

7

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30 July 2017

publication date

1 September 2000

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30 July 2017

published in

Experimental Gerontology

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30 July 2017

volume

35

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30 July 2017

issue

6-7

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30 July 2017

page(s)

831-841

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Familial Alzheimer's disease-linked presenilin 1 variants elevate Abeta1-42/1-40 ratio in vitro and in vivo

30 July 2017

cites work

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

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https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Amyloid, the presenilins and Alzheimer's disease

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https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes

1 reference

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7 January 2021

Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

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7 January 2021

Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of Alzheimer disease

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Expression in brain of amyloid precursor protein mutated in the alpha-secretase site causes disturbed behavior, neuronal degeneration and premature death in transgenic mice.

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Transgenic mice expressing an alpha-secretion mutant of the amyloid precursor protein in the brain develop a progressive CNS disorder

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Aggressive behaviour in transgenic mice expressing APP is alleviated by serotonergic drugs

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7 January 2021

Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain

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https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Premature death in transgenic mice that overexpress a mutant amyloid precursor protein is preceded by severe neurodegeneration and apoptosis

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https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

The cell biology of beta-amyloid precursor protein and presenilin in Alzheimer's disease

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7 January 2021

Prominent axonopathy in the brain and spinal cord of transgenic mice overexpressing four-repeat human tau protein

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Expression of human apolipoprotein E4 in neurons causes hyperphosphorylation of protein tau in the brains of transgenic mice

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

Prominent cerebral amyloid angiopathy in transgenic mice overexpressing the london mutant of human APP in neurons.

1 reference

https://api.crossref.org/works/10.1016%2FS0531-5565%2800%2900149-2

7 January 2021

10.1016/S0531-5565(00)00149-2

Identifiers

DOI

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30 July 2017

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