• aged mice exhibit reduced amyloid plaques compared to Apoe^{tm2(APOE_i3)Yhg}/Apoe^{tm2(APOE_i3)Yhg} Tg(PDGFB-APPSwInd)20Lms mice

• aged mice exhibit reduced amyloid plaques compared to Apoe^{tm2(APOE_i3)Yhg}/Apoe^{tm2(APOE_i3)Yhg} Tg(PDGFB-APPSwInd)20Lms mice

• aged mice exhibit reduced amyloid plaques compared to Apoe^{tm3(APOE_i4)Yhg}/Apoe^{tm3(APOE_i4)Yhg} Tg(PDGFB-APPSwInd)20Lms mice

• aged mice exhibit reduced amyloid plaques compared to Apoe^{tm3(APOE_i4)Yhg}/Apoe^{tm3(APOE_i4)Yhg} Tg(PDGFB-APPSwInd)20Lms mice

• increased

• neuron loss in the CA3 region at 17 days relative to controls

• plaque levels are doubled in the hippocampus and mid frontal cortex relative to controls at 17 months of age but normal at 12 months

• plasma amyloid levels are increased 51% at 17 months

• plaque levels are doubled in the hippocampus and mid frontal cortex relative to controls at 17 months of age but normal at 12 months

• plasma amyloid levels are increased 51% at 17 months

• increased

• mice do not exhibit premature death as do Tg(PDGFB-APPSwInd)20Lms mice (J:141084)

• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)

• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice that are not as severe as in Tg(PDGFB-APPSwInd)20Lms mice

• mice exhibit a complete or partial recovery of the learning deficits observed in Tg(PDGFB-APPSwInd)20Lms mice with improved target crossing in a Morris water maze

• mice do not exhibit premature death as do Tg(PDGFB-APPSwInd)20Lms mice (J:141084)

• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)

• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice that are not as severe as in Tg(PDGFB-APPSwInd)20Lms mice

• mice exhibit a complete or partial recovery of the learning deficits observed in Tg(PDGFB-APPSwInd)20Lms mice with improved target crossing in a Morris water maze

• mice show normal spatial learning and object-recongition memory, at levels similar to non-transgenic controls (J:121330)

• mice show no signs of hyperactivity (J:121330)

• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt

• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt

• mice show neuritic dystrophy around amyloid plaques

• aberrant sprouting of hippocampal axons is observed in transgenic mice

• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous or wild-type for Mapt

• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous or wild-type for Mapt

• aberrant sprouting of hippocampal axons is observed in transgenic mice

• mice show no signs of hyperactivity (J:121330)

• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt

• in the hidden platform version of the Morris water maze, non-trangenic controls, regardless of Mapt genotype learn the task over 3 days, whereas transgenic mice heterozygous for Mapt^tm1Hnd show show impaired learning compared to controls but less impairment than transgenic mice with normal Mapt expression

• in probe trials where the platform is removed, mice show delayed learning, compared to non transgenic controls or transgenic mice with wild-type Mapt, with more target than non-target crossings after 5 days of training

• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt

• mice show neuritic dystrophy around amyloid plaques

• aberrant sprouting of hippocampal axons is observed in transgenic mice

• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics null or wild-type for Mapt

• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics null or wild-type for Mapt

• aberrant sprouting of hippocampal axons is observed in transgenic mice

• 6-8 month old mutants show increased latencies to locate the hidden platform in the Morris water maze indicating a learning deficit

• 12- and 18-month old mutants show impaired probe trial performance, indicating a memory impairment

• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels

• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness

• middle cerebral arteries show a 50% loss of ability to dilate in response to acetylcholine and calcitonin gene-related peptide compared to wild-type vessels

• arterial dysfunction is not due to oxidative stress

• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine

• however, contractile response of arteries to endothelin-1 is normal

• middle cerebral arteries show a 50% loss of ability to dilate in response to acetylcholine and calcitonin gene-related peptide compared to wild-type vessels

• arterial dysfunction is not due to oxidative stress

• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine

• however, contractile response of arteries to endothelin-1 is normal

• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness

• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels

• mutants exhibit activated GFAP-positive astrocytes in the cortex; activated astrocytes are distributed in clusters as well as diffusely throughout the cortex

• mutants exhibit significant collagen accumulation in the surface pial membrane, resulting in increased thickness

• about 22-23% reduction in the number of cortical cholinergic fibers in adults and aged-mutants

• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques

• mutants exhibit increased levels of soluble and insoluble amyloid beta(1-40) and amyloid beta(1-42) between 6-8 and 12 months of age and further increases in amyloid beta(1-40) at 18 months of age, in the cortex

• glucose uptake is impaired in activated somatosensory cortex of aged mutants after whisker stimulation

• gradual loss of the neuronally-driven hemodynamic response to sensory whisker stimulation

• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels

• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques

• mutants exhibit increased levels of soluble and insoluble amyloid beta(1-40) and amyloid beta(1-42) between 6-8 and 12 months of age and further increases in amyloid beta(1-40) at 18 months of age, in the cortex

• attenuated premature death at 6 months relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates

• microgliosis is reduced

• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates

• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice

• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~50% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaque burden is reduced by ~50%

• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~50% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaque burden is reduced by ~50%

• attenuated premature death at 6 months relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates

• microgliosis is reduced

• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates

• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice

• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~90% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaques are almost absent

• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~90% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaques are almost absent

• at 6 months and 12 to 16 months of age, 30% fewer pyramidal cells in the entorhinal cortex express Reelin than in wild-type mice

• however, no neuron loss is observed

• dystrophic neurites are associated with plaques

• mice develop amyloid peptide deposits by 5-7 months of age

• mice develop amyloid peptide deposits by 5-7 months of age

• high rate of premature (6 months or earlier) death (J:87150)

• mice show premature death of unclear etiology with >15% mortality exhibited by 6 months, compared to all other genotypes (J:121330)

• mice are abnormally sensitive to pentylenetetrazole (PTZ)-induced seizures with 20% suffering fatal status epilepticus at a PTZ dose not lethal in non-transgenic controls

• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice

• at 4-7 months of age, mice transgenic mice with wild-type Mapt expression take longer to locate the platform in the cued version of the Morris water maze test compared to transgenic mice heterozygous or homozygous for Mapt deletion

• in the hidden platform version of the Morris water maze, non-trangenic controls, regardless of Mapt genotype learn the task over 3 days, whereas transgenic mice with wild-type expression of Mapt show no evidence of learning (J:121330)

• in probe trials where the platform is removed, mice show no learning, displaying no significantly elevated crossings of the target quadrant after 5 days of training (J:121330)

• in a Morris water maze, mice fail to favor the target platform location unlike wild-type mice (J:141084)

• mice show hyperactivity in the Y-maze, a new cage, and elevated-plus maze compared to other transgenic mice or non-transgenic controls; this persists in mice 12-16 months of age (J:121330)

• mice are abnormally sensitive to pentylenetetrazole (PTZ)-induced seizures with 20% suffering fatal status epilepticus at a PTZ dose not lethal in non-transgenic controls

• mice show neuritic dystrophy around amyloid plaques

• aberrant sprouting of hippocampal axons is observed in transgenic mice

• diffuse immunoreactive amyloid deposits detected in dentate gyrus and neocortex of mice aged 5 to 7 months old (J:62290)

• all mice exhibit plaques by age 8 to 10 months (J:62290)

• soluble and insoluble Abeta-40 and -42 peptide deposits at 6-10 months (J:87150)

• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous null for Mapt (J:121330)

• neurodegeneration is indicated by an age dependent decrease in density of synaptophysin-immunoreactive presynaptic terminals

• diffuse immunoreactive amyloid deposits detected in dentate gyrus and neocortex of mice aged 5 to 7 months old (J:62290)

• all mice exhibit plaques by age 8 to 10 months (J:62290)

• soluble and insoluble Abeta-40 and -42 peptide deposits at 6-10 months (J:87150)

• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous null for Mapt (J:121330)

• aberrant sprouting of hippocampal axons is observed in transgenic mice