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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Apptm1Ck
targeted mutation 1, Christoph Kohler
MGI:3609234
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Apptm1Ck/Apptm1Ck involves: 129 MGI:5581645
cx2
Apptm1Ck/Apptm1Ck
Psen1tm1Mpm/Psen1tm1Mpm
Tg(MAPT)8cPdav/0
B6.Cg-Psen1tm1Mpm Apptm1Ck Tg(MAPT)8cPdav MGI:5581681
cx3
Apptm1Ck/Apptm1Ck
Psen1tm1Mpm/Psen1tm1Mpm
involves: 129 * 129S1/Sv * 129X1/SvJ MGI:4847595
cx4
Apptm1Ck/Apptm1Ck
Tg(PDGFB-PSEN1M146L)2Jhd/0
involves: 129 * Black Swiss * C57BL/6 * DBA/2 * SW MGI:3625136
cx5
Apptm1Ck/Apptm1Ck
Tg(PDGFB-PSEN1)1Jhd/0
involves: 129 * Black Swiss * C57BL/6 * DBA/2 * SW MGI:5581665


Genotype
MGI:5581645
hm1
Allelic
Composition
Apptm1Ck/Apptm1Ck
Genetic
Background
involves: 129
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apptm1Ck mutation (0 available); any App mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in the elevated plus maze, mice show decreased open time and increased closed time

nervous system
• corticotropin releasing factor levels are increased in the lateral dorsal bed nucleus of the stria terminalis




Genotype
MGI:5581681
cx2
Allelic
Composition
Apptm1Ck/Apptm1Ck
Psen1tm1Mpm/Psen1tm1Mpm
Tg(MAPT)8cPdav/0
Genetic
Background
B6.Cg-Psen1tm1Mpm Apptm1Ck Tg(MAPT)8cPdav
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apptm1Ck mutation (0 available); any App mutation (22 available)
Psen1tm1Mpm mutation (2 available); any Psen1 mutation (28 available)
Tg(MAPT)8cPdav mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice show increased contextual freezing frequency at 4 and 12 months of age
• however, cued freezing frequency is unaffected and mice do not exhibit spatial memory deficits in the Morris water maze
• in the elevated plus maze, 4 month old mice spend less time on the open arm, indicating increased anxiety
• however, mice show normal nociception in the hot plate assay
• mice show slightly higher pre-shock freezing frequency and increased contextual freezing frequency at 4 and 12 months of age, indicating exaggerated fear response
• in the open field, the total travel distance is reduced at 12, but not 4, months of age, indicating age-dependent reduced activity

homeostasis/metabolism
• mice exhibit amyloid beta plaques on the outer edge of the cortex at 18-22 months of age which progress into inner layers of the cortex and hippocampus by 26-29 months of age

nervous system
• mice exhibit amyloid beta plaques on the outer edge of the cortex at 18-22 months of age which progress into inner layers of the cortex and hippocampus by 26-29 months of age
• increase in phosphorylated tau in the cortex and hippocampus

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:209782




Genotype
MGI:4847595
cx3
Allelic
Composition
Apptm1Ck/Apptm1Ck
Psen1tm1Mpm/Psen1tm1Mpm
Genetic
Background
involves: 129 * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apptm1Ck mutation (0 available); any App mutation (22 available)
Psen1tm1Mpm mutation (2 available); any Psen1 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice exhibit decreased amyloid load compared with Apptm3.1Zhe Psen1tm1Mpm double homozygotes
• corticotropin releasing factor levels are increased in the lateral dorsal bed nucleus of the stria terminalis and the paraventricular nucleus

homeostasis/metabolism
• mice exhibit an increase in resting levels of circulating corticosterone
• mice exhibit decreased amyloid load compared with Apptm3.1Zhe Psen1tm1Mpm double homozygotes

behavior/neurological
• mice show increased freezing in the context in which they received the shock compared to wild-type mice but show similar levels of freezing as wild-type mice in cued fear (in response to sound), indicating increased contextual fear
• however, hot plate assay shows normal nociception
• in the alternation T-maze test, mice show decreased alternation, indicating reduced working memory
• in the elevated plus maze, mice spend more time in the closed arms and less time in the open arms and make fewer entries into the open arms and navigate less distance on the open arms, indicating increased levels of anxiety
• in the light-dark box test, mice spend more time in the closed portion of the box and less time in the open side, make fewer entries to the light side of the box, and spend on average more time on each visit to the dark side, suggesting an increase in hiding behavior and reduction in exploring
• mice show increased freezing in the context in which they received the shock compared to wild-type mice but show similar levels of freezing as wild-type mice in cued fear (in response to sound)
• during the cued trial, mice show increased baseline freezing levels in the 3 minutes before presentation of sound, however increased baseline freezing is not seen before mice are shocked

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:191170




Genotype
MGI:3625136
cx4
Allelic
Composition
Apptm1Ck/Apptm1Ck
Tg(PDGFB-PSEN1M146L)2Jhd/0
Genetic
Background
involves: 129 * Black Swiss * C57BL/6 * DBA/2 * SW
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apptm1Ck mutation (0 available); any App mutation (22 available)
Tg(PDGFB-PSEN1M146L)2Jhd mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• microglia are seen associated with compact plaques
• mice develop two types of amyloid plaques beginning at 9 months of age, either compact, typically round (compact) plaque which are seen at early stages or fluffy amyloid beta material (diffuse) plaque which are seen at later stages (J:102542)
• at 12 months of age, plaques are seen in the frontal, parietal, occipital, cingulate, and temporal cortices, in the hippocampus, and in the white matter, most often in the corpus callosum (J:102542)
• at 18 months, amyloid beta deposits develop in the entorhinal and piriform cortices such that 21 months, density is high in the piriform cortex but relatively low in the entorhinal cortex (J:102542)
• at 18 months, plaques spread to extracortical sites, mainly to the striatum and septum and at 21 months, they are seen in the colliculi (thalamus, amygdala, olfactory bulb, and olfactory nucleus but not in the cerebellum, pons, or medulla oblongata (J:102542)
• mice develop vascular amylod-beta deposits in leptomeningeal vessels and their larger intracortical branches at 12 months of age (J:102542)
• however, mice do not develop neurofibrillary tangles or show signs of neurodegeneration (J:102542)
• amyloid plaques are detected in the brains of these mutant transgenic mice but not in App transgenic or App Tg(PDGFB-PSEN1M146L)2Jhd transgenic mutant mice up to 20 months of age (J:102879)
• activated astrocytes are seen associated with plaques
• mice develop abnormal cholinergic fiber aggregates and enlarged terminals after 12 months of age (J:102542)
• in 1-year old animals, a relatively high number of cholinergic fiber aggregates in the cortex are observed in transgenic; at 20 months of age, a few such areas of densed cholinergic fiber aggregations are observed in other APP-targeted mice (J:102879)
• cholinergic fibers of large diameter are seen in layer 1 of the entorhinal cortex in mutant transgenic mice more prominently than in the other strains, but such fibers are present even in controls (J:102879)
• clusters of ballooned and spherical acetylcholine-immunoreactive terminals are observed in the periphery of compact amyloid plaques around the amyloid core in 12-month old animals, and numbers increase with age and plaque load (J:102879)

homeostasis/metabolism
• mice develop two types of amyloid plaques beginning at 9 months of age, either compact, typically round (compact) plaque which are seen at early stages or fluffy amyloid beta material (diffuse) plaque which are seen at later stages (J:102542)
• at 12 months of age, plaques are seen in the frontal, parietal, occipital, cingulate, and temporal cortices, in the hippocampus, and in the white matter, most often in the corpus callosum (J:102542)
• at 18 months, amyloid beta deposits develop in the entorhinal and piriform cortices such that 21 months, density is high in the piriform cortex but relatively low in the entorhinal cortex (J:102542)
• at 18 months, plaques spread to extracortical sites, mainly to the striatum and septum and at 21 months, they are seen in the colliculi (thalamus, amygdala, olfactory bulb, and olfactory nucleus but not in the cerebellum, pons, or medulla oblongata (J:102542)
• mice develop vascular amylod-beta deposits in leptomeningeal vessels and their larger intracortical branches at 12 months of age (J:102542)
• however, mice do not develop neurofibrillary tangles or show signs of neurodegeneration (J:102542)
• amyloid plaques are detected in the brains of these mutant transgenic mice but not in App transgenic or App Tg(PDGFB-PSEN1M146L)2Jhd transgenic mutant mice up to 20 months of age (J:102879)

hematopoietic system
• microglia are seen associated with compact plaques

immune system
• microglia are seen associated with compact plaques




Genotype
MGI:5581665
cx5
Allelic
Composition
Apptm1Ck/Apptm1Ck
Tg(PDGFB-PSEN1)1Jhd/0
Genetic
Background
involves: 129 * Black Swiss * C57BL/6 * DBA/2 * SW
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apptm1Ck mutation (0 available); any App mutation (22 available)
Tg(PDGFB-PSEN1)1Jhd mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• areas of higher density of cholinergic fibers in the cortex at 20 months of age
• however, mice do not form amyloid beta plaques





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last database update
09/27/2016
MGI 6.05
The Jackson Laboratory