Research Models
Selected Results
2 Models
Name | Other Names | Strain Name | Genetic Background | Gene | Mutation | Modification Info | Modification | Disease | Neuropathology | Behavior/Cognition | Other Phenotype | Availability | Primary Paper | Visualization | |
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Mouse Models (2) |
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C57BL/6J | APP | APP K670_M671delinsNL (Swedish), APP T714I (Austrian) | Transgene-expressing mutant APP with the Swedish mutation (K670N/M671L) and the Austrian mutation (T714I) under the control of the Thy1.2 promoter. | APP: Transgenic | Alzheimer's Disease | Progressive amyloid deposition in the cerebral cortex by approximately 9-12 months. | Unknown. | Optogenetic stimulation induced epileptic seizures. | Unknown | Yamada et al., 2009 | Yes | ||||
AppSAA, AppSAA Knock-in, AppSAA KI, APP-SAA KI, hAbetaSAA, hAbetaSwe,Arc,Aus | B6(Cg)-Apptm1.1Dnli/J | C57BL/6J | App | APP K670_M671delinsNL (Swedish), APP E693G (Arctic), APP T714I (Austrian) | Homologous recombination was used to humanize the Aβ sequence and introduce the FAD-linked Swedish, Arctic, and Austrian mutations into the murine App gene. | App: Knock-In | Alzheimer's Disease | Homozygotes: Amyloid plaques and plaque-associated microgliosis from 4 months of age; cerebral amyloid angiopathy and dystrophic neurites from 8 months of age. Heterozygotes: Amyloid plaques at 16 months of age. | Unknown. | Increased levels of CSF total tau and neurofilament light chain in AppSAA homozygous mice at 8 months of age. Significant alterations of the transcriptomes and lipidomes in microglia of AppSAA homozygotes. | Available from The Jackson Laboratory Stock# 034711. | Xia et al., 2021 | Yes |
2 Visualizations
AD-related Research Models
Phenotypes Examined
- Plaques
- Tangles
- Neuronal Loss
- Gliosis
- Synaptic Loss
- Changes in LTP/LTD
- Cognitive Impairment
When visualized, these phenotypes will distributed over a 18 month timeline demarcated at the following intervals: 3mo, 6mo, 9mo, 1yr, 15mo, 18mo+.
A7 APP transgenic
Observed
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Plaques at 39
These mice develop progressive amyloid deposition in the cerebral cortex by 9-12 months. By 21 months of age amyloid pathology is extensive.
Absent
No Data
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Tangles at
No data.
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Neuronal Loss at
No data.
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Gliosis at
No data.
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Synaptic Loss at
No data.
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Changes in LTP/LTD at
No data.
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Cognitive Impairment at
No data.
Genes | Mutations | Modification | Disease | Neuropathology | Behavior/Cognition |
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APP | APP K670_M671delinsNL (Swedish), APP T714I (Austrian) | APP: Transgenic | Alzheimer's Disease | Progressive amyloid deposition in the cerebral cortex by approximately 9-12 months. |
Unknown. |
AppSAA Knock-in
Observed
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Plaques at 16
Amyloid plaques seen in AppSAA homozygous mice from 4 months of age and heterozygous mice at 16 months of age.
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Gliosis at 16
Plaque-associated microgliosis observed by 4 months of age.
Absent
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Tangles at
AT8-positive dystrophic neurites, but no neurofibrillary tangles, detected in AppSAA homozygous mice at 8 months of age.
No Data
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Neuronal Loss at
No data.
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Synaptic Loss at
No data.
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Changes in LTP/LTD at
No data.
-
Cognitive Impairment at
No data.
Genes | Mutations | Modification | Disease | Neuropathology | Behavior/Cognition |
---|---|---|---|---|---|
App | APP K670_M671delinsNL (Swedish), APP E693G (Arctic), APP T714I (Austrian) | App: Knock-In | Alzheimer's Disease | Homozygotes: Amyloid plaques and plaque-associated microgliosis from 4 months of age; cerebral amyloid angiopathy and dystrophic neurites from 8 months of age. Heterozygotes: Amyloid plaques at 16 months of age. |
Unknown. |