All Phenotypes Tg(APPSwe,tauP301L)1Lfa MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cx1	Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/?	B6.Cg-Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa	MGI:5003275
cx2	Cx3cr1^tm1Litt/Cx3cr1^tm1Litt Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/0 Tg(Thy1-YFP)HJrs/0	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:4834196
cx3	Cx3cr1^tm1Litt/Cx3cr1⁺ Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/0 Tg(Thy1-YFP)HJrs/0	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:4834197
cx4	Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Tg(APPSwe,tauP301L)1Lfa	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3720782
cx5	Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/?	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3720789

Allelic Composition	Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/?
Genetic Background	B6.Cg-Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psen1^tm1Mpm mutation (4 available); any Psen1 mutation (48 available)
Tg(APPSwe,tauP301L)1Lfa mutation (3 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

abnormal behavior ( J:170670 )

• mutants attend less accurately to short, spatially unpredictable stimuli when the attentional demand of the task is high and also show a general tendency to make more perseverative responses than wild-type mice

• mutants initially respond as accurately as wild-type mice, however subsequently they fail to sustain their attention over the duration of the task, indicating reduced vigilance, or ability to sustain attention over a long period of time

• treatment of mice with the cholinesterase inhibitor donepezil results in an enhanced ability to sustain attention

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Alzheimer's disease		DOID:10652		J:170670

Allelic Composition	Cx3cr1^tm1Litt/Cx3cr1^tm1Litt Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/0 Tg(Thy1-YFP)HJrs/0
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cx3cr1^tm1Litt mutation (6 available); any Cx3cr1 mutation (45 available)
Psen1^tm1Mpm mutation (4 available); any Psen1 mutation (48 available)
Tg(APPSwe,tauP301L)1Lfa mutation (3 available)
Tg(Thy1-YFP)HJrs mutation (3 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

nervous system phenotype ( J:159680 )

N	• mice do not exhibit the neuron loss or increase in microglial density and migration velocity observed in Cx3cr1^tm1Litt/Cx3cr1⁺ Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice

Allelic Composition	Cx3cr1^tm1Litt/Cx3cr1⁺ Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/0 Tg(Thy1-YFP)HJrs/0
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal microglial cell morphology ( J:159680 )

• microglial density increases over time around lost neurons unlike in Cx3cr1^tm1Litt/Cx3cr1^tm1Litt Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice

abnormal microglial cell physiology ( J:159680 )

• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1^tm1Litt heterozygotes and homozygotes

neuron degeneration ( J:159680 )

• of YFP+ layer III neurons at 4 to 6 months

immune system

abnormal microglial cell morphology ( J:159680 )

• microglial density increases over time around lost neurons unlike in Cx3cr1^tm1Litt/Cx3cr1^tm1Litt Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice

abnormal microglial cell physiology ( J:159680 )

• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1^tm1Litt heterozygotes and homozygotes

hematopoietic system

abnormal microglial cell morphology ( J:159680 )

• microglial density increases over time around lost neurons unlike in Cx3cr1^tm1Litt/Cx3cr1^tm1Litt Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice

abnormal microglial cell physiology ( J:159680 )

• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1^tm1Litt heterozygotes and homozygotes

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

abnormal learning/memory/conditioning ( J:99604 )

• in Morris water mazed, learning of task is normal but retention is impaired; 6-month old mice require 6 days of training to achieve escape latency of >20 seconds, compared to 3 days in 2 month old control mice

• at 4 and 6 months, mice show longer escape latencies in the first daily trial relative to the last trial of the previous training day indicating day-to-day retention impairment; 2-month old mice do not show this impairment in retention

• short- (1.5 hr posttraining) and long-term (24 hr posttraining) spatial recognition memory in probe trials are impaired at 6 months, whereas 4-month old mice show similar performance at 1.5 hours and impaired retention at 24 hours

• after clearance of intraneuronal Abeta using antibodies, early retention deficits are ablated, whereas long-term retention remains impaired

abnormal contextual conditioning behavior ( J:99604 )

• at 6 months, naive and trained mice display significantly impaired long- and short-term retention for contextual fear; at 4 months, mice have normal retention for short-term (1.5 hr) contextual fear but impaired memory of contextual fear at 24 hours

nervous system

amyloid beta deposits ( J:99604 )

• at 6 months, extracellular Abeta plaques are observed in the cerebral cortex, and intracellular accumulation is seen in pyramidal neurons of the CA1 region of hippocampus and within basolateral amygdala and cortical neurons

• prominent intraneuronal Abeta accumulation is present at 4 months, preceding extracellular amyloid plaque formation

• treatment of mice with antibodies to Abeta results in clearance of intraneuroanl Abeta in hippocampus and cortex, but not in amygdala

homeostasis/metabolism

amyloid beta deposits ( J:99604 )

• prominent intraneuronal Abeta accumulation is present at 4 months, preceding extracellular amyloid plaque formation

• treatment of mice with antibodies to Abeta results in clearance of intraneuroanl Abeta in hippocampus and cortex, but not in amygdala

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Alzheimer's disease		DOID:10652		J:99604

Allelic Composition	Psen1^tm1Mpm/Psen1^tm1Mpm Tg(APPSwe,tauP301L)1Lfa/?
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psen1^tm1Mpm mutation (4 available); any Psen1 mutation (48 available)
Tg(APPSwe,tauP301L)1Lfa mutation (3 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

amyloid beta deposits ( J:107286 )

• Abeta oligomers begin to accumulate between 2 and 6 months of age, with continued age-dependent increase observed between 12 and 20 months

• intraneuronal oligomers are detected at 4-6 months of age

neurofibrillary tangles ( J:107286 )

• tau pathology is detected initially by 6 months of age, and tangle pathology is advanced by 20 months

homeostasis/metabolism

amyloid beta deposits ( J:107286 )

• Abeta oligomers begin to accumulate between 2 and 6 months of age, with continued age-dependent increase observed between 12 and 20 months

• intraneuronal oligomers are detected at 4-6 months of age

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