General Information:

Id: 652
Diseases: Alzheimer disease - [OMIM]
Mus musculus
PS1-conditioned/PS2-conventioned double-knockout mouse, (PS1/PS2-KO)
brain
article
Reference: Chen Q et al.(2008) Loss of presenilin function causes Alzheimers disease-like neurodegeneration in the mouse. J. Neurosci. Res. 86: 1615-1625 [PMID: 18189321]

Interaction Information:

Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3455

organism model

PS1/PS2-KO mouse

increases_activity of

phenotype

neurodegeneration

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3456

organism model

PS1/PS2-KO mouse

decreases_activity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3458

organism model

PS1/PS2-KO mouse

NOT increases_quantity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3462

organism model

PS1/PS2-KO mouse

increases_activity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3463

organism model

PS1/PS2-KO mouse

increases_activity of

phenotype

gliosis

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3465

organism model

PS1/PS2-KO mouse

increases_quantity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3466

gene/protein mutant

PSEN1-mut

increases_activity of

phenotype

neurodegeneration

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3467

gene/protein mutant

PSEN2-mut

increases_activity of

phenotype

neurodegeneration

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3470

gene/protein mutant

PSEN1-mut

affects_activity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3472

gene/protein mutant

PSEN2-mut

affects_activity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3473

gene/protein mutant

PSEN1-mut

increases_activity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3475

gene/protein mutant

PSEN2-mut

increases_activity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3476

gene/protein mutant

PSEN1-mut

increases_activity of

phenotype

gliosis

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3478

gene/protein mutant

PSEN2-mut

increases_activity of

phenotype

gliosis

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3480

gene/protein mutant

PSEN1-mut

affects_quantity of

in brain
Comment Conditional knockout of PS1 from the adult stage in the forebrain of mice with the PS2 null mutation triggers robust AD-like neurodegeneration including brain shrinkage, cortical and hippocampal atrophy, ventricular enlargement, severe neuronal loss, gliosis, tau hyperphosphorylation, neurofillament tanglelike structures, and intracellular filaments. Learning and memory functions in these mice are almost completely lost. There is no beta-amyloid deposition.
Formal Description
Interaction-ID: 3481

gene/protein mutant

PSEN2-mut

affects_quantity of

in brain
Comment Presenilin dysfunction can directly cause neurodegeneration without the involvement of beta-amyloid.
Formal Description
Interaction-ID: 3483

gene/protein mutant

PSEN1-mut

NOT affects_activity of

gene/protein

Amyloid beta peptide