Mouse Genome Informatics
cx1
    Mapttm1(EGFP)Klt/Mapttm1(EGFP)Klt
Tg(MAPT)8cPdav/0

B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
behavior/neurological
• 6 month old mutants exhibit slower visuospatial learning than control mice
• in the visuospatial re-learning test performed at 7, 8, 9, and 15 months of age, mutants exhibit a decrease in the speed of re-learning the task compared to controls
• however, mutants perform better than Tg(APPswe,PSEN1dE9)85Dbo mice on the visuospatial re-learning test at 9 and 18 months of age

taste/olfaction
N
• mutants do not exhibit Alzheimer's disease-related impairment in olfactory performance in tests based on an operant conditioning procedure and in tests based on a habituation/dishabituation procedure (J:172426)

nervous system

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:172426


Mouse Genome Informatics
cx2
    Apptm1Ck/Apptm1Ck
Psen1tm1Mpm/Psen1tm1Mpm
Tg(MAPT)8cPdav/0

B6.Cg-Psen1tm1Mpm Apptm1Ck Tg(MAPT)8cPdav
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
behavior/neurological
• 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
• 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 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 IDRef(s)
Alzheimer Disease; AD 104300 J:209782


Mouse Genome Informatics
cx3
    Mapttm1(EGFP)Klt/Mapttm1(EGFP)Klt
Tg(MAPT)8cPdav/?

involves: 129S4/SvJae * C57BL/6 * Swiss Webster
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• phosphorylated tau accumulates in neuronal cell bodies and dendrites of the hippocampus and neocortex as early as 3 months of age
• in particular, accumulations occur in entorhinal cortex, ventromedial hypothalamus, medial septum and the nucleus of the horizontal limb of the diagonal band
• increase in tau phosphorylation occurs at serine 202, threonine 231 and serine 235 as determined by immunoblot
• tau aggregates in the proximal dendrites have an average width of 15 nm and are not densely packed
• insoluble tau is present in both 2 and 9 month old mice
• paired helical filaments are observed in 9, 12 and 14 month old mice
• cells in the cortex and hippocampus appear irregularly shaped, often with distorted processes in 13 month old mice

hematopoietic system
• splenic red pulp is largely obliterated
• splenic white pulp contains follicles that are larger and more irregular in shape than normal follicles and are often fused with adjacent follicles

immune system
• splenic red pulp is largely obliterated
• splenic white pulp contains follicles that are larger and more irregular in shape than normal follicles and are often fused with adjacent follicles

renal/urinary system
• kidney glomeruli are dilated probably due to obstruction from the amyloid in the lumen or walls of medullary tubules especially in the papilla

tumorigenesis
• malignant lymphoma in the spleen and lymph nodes are seen in some mutants
• megakaryocytes are numerous is some spleens, suggesting a relation to megakaryocytic leukemia
• splenic architecture is replaced by proliferated immature mononuclear cells arranged in follicular aggregates indicating follicular lymphoma

homeostasis/metabolism
• some mutants older than 18 months exhibit amyloid deposits in the spleen, kidneys, liver, ovary and/or heart
• amyloid is deposited concentrically in the perifollicular sheath, partly or completely encircling the follicles in the spleen
• in the liver, amyloid deposit is in the walls of sinusoids or central veins
• in the kidney, amyloid deposits are seen in the glomeruli
• amyloid deposits in the heart are not composed of amyloid-beta peptide, but rather amyloid A

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:84638 , J:174270