543 research outputs found
hAPP-J20 mice exhibit hyperactivity.
No full text<p>hAPP-J20 mice did not spend significantly more time in the open arm of the elevated plus maze at (A) 16 or (B) 24 weeks of age indicating no difference in anxiety levels compared to age-matched WT littermates. However, hAPP-J20 mice did show hyperactivity at (C) 16 and (D) 24 weeks of age as indicated by the total distance traveled in the open field test. Each value represents the mean ± standard error of the mean (SEM). *<i>p</i><0.05, ***<i>p</i><0.001.</p
Quantification of CD68-positive activated microglia in hAPP-J20 mice.
No full text<p>CD68-positive microglia were observed in the hippocampus of (A) WT mice compared to (B) their hAPP-J20 littermates at 36 weeks of age. Quantification of CD68-positive cell numbers revealed significant increases in cell numbers at 24 (<i>p</i><0.01) and 36 weeks of age (<i>p</i><0.01) in hAPP-J20 mice compared to their age-matched WT littermates. Further, a significant increase in CD68 microglia occurred between 6 week and 36-week-old hAPP-J20 mice (<i>p</i><0.01). Each value represents the mean ± standard error of the mean (SEM). **<i>p</i><0.01.</p
Spatial learning and memory deficits in hAPP-J20 mice.
No full text<p>(A) Schematic representation of the radial arm maze. Filled circles represent the baited arms (B) hAPP-J20 mice had significantly impaired spatial reference memory and learning at 16 weeks of age (<i>p</i><0.05) when compared to age-matched WT littermates. (C) 16-week-old hAPP-J20 mice had significant deficits in spatial reference memory and learning retention (<i>p</i><0.05) when compared to age-matched WT littermates. (D) 24-week-old hAPP-J20 mice also showed significantly impaired spatial reference memory and learning (<i>p</i><0.05) when compared to age-matched WT littermates. (E) Spatial reference memory and learning retention was significantly impaired in 24-week-old hAPP-J20 mice (<i>p</i><0.05). Each value represents the mean ± standard error of the mean (SEM). *<i>p</i><0.05, **<i>p</i><0.01.</p
Contextual fear conditioning is not impaired in hAPP-J20 mice.
No full text<p>(A) No deficits were seen in the percentage of freezing in 28 and 36-week-old hAPP-J20 mice when compared to age-matched WT littermates. (B) A retention test, performed at 40 weeks, also revealed no deficits in the percentage of freezing in 36-week-old hAPP-J20 mice when compared to age-matched controls. Each value represents the mean ± standard error of the mean (SEM).</p
5–7 month old hAPP mice exhibit impairments in neurogenesis.
No full text<p>A, Micrographs of doublecortin immunostaining in coronal brain sections from NTG and hAPP mice. B, High magnification micrograph illustrating doublecortin-positive neuroblasts (Nb) and immature neurons (ImN). C–D, Quantification of doublecortin expression demonstrates significant decreases in neuroblasts (C) and immature neurons (D) in hAPP mice relative to NTG controls. E–F, BrdU-labeling of dividing cells in the subgranular zone confirms a decrease in cell division in hAPP mice compared to NTG mice. Arrowheads, BrdU-labeled cells. n = 12/genotype. *p<0.05, ***p<0.001.</p
13–15 month old hAPP mice display subtle depressive behavior.
No full text<p>A, In the tail suspension test, hAPP mice exhibit decreased latency to the first bout of immobility relative to NTG controls. B, No significant difference between hAPP and NTG mice in the total time spent immobile during the 6-minute tail suspension test trial. C, hAPP mice become immobile sooner than do NTG mice during the tail suspension trial. D, Both NTG and hAPP mice demonstrate decreased latency to the first bout of immobility in response to a repeated tail suspension test. E, NTG mice increase the time spent immobile during a repeated tail suspension test, whereas there is no change in hAPP mice. F, Analyzing just the first three minutes of the tail suspension test reveals that hAPP mice spend more time immobile during the initial portion of the test. G, Analysis of the first three minutes of the tail suspension test at baseline and at the 24 hr trial confirms that NTG, but not hAPP, mice increase the time spent immobile upon repeated testing. n = 11–12/genotype. *p<0.05, ** p<0.01, ***p<0.001.</p
13–15 month old hAPP mice exhibit decreased neurogenesis.
No full text<p>A, Micrographs of doublecortin immunostaining in coronal brain sections from NTG and hAPP mice. B, High magnification micrograph illustrating doublecortin-positive neuroblasts (Nb) and immature neurons (ImN). C–D, Quantification of doublecortin expression demonstrates significant decreases in neuroblasts (C) and immature neurons (D) in hAPP mice relative to NTG controls. E–F, BrdU labeling of dividing cells in the subgranular zone demonstrates fewer dividing cells in the subgranular zone of hAPP mice. Arrowheads, BrdU-labeled cells. n = 11–12/genotype. *p<0.05, ***p<0.001.</p
Quantification of hippocampal neuronal populations in hAPP-J20 mice.
No full text<p>(A) No cell loss was detected in the CA3 region of the hippocampus of hAPP-J20 mice at 6, 24 and 36 weeks of age. (B) No cell loss in the CA1 region was detected at 6 weeks, however, 12 (<i>p</i><0.05), 24 (<i>p</i><0.05) and 36-week-old (<i>p</i><0.001) mice showed significant cell loss when compared to aged-matched WT controls. Moreover, cell loss was significantly different between 6 and 36-week-old hAPP-J20 mice (<i>p</i><0.001). Cell loss in the CA1 region can be qualitatively seen between (C) WT and (D) 36-week-old hAPP-J20 mice. Each value represents the mean ± standard error of the mean (SEM). *<i>p</i><0.05, ***<i>p</i><0.001.</p
Age-dependent Aβ expression and plaque deposition in the hAPP-J20 mice.
No full text<p>(A) 6E10 immunohistochemistry illustrated increased neuronal Aβ from 6 to 12, 24 and 36-week-old hAPP-J20 mice (quantified in E). (B) Aβ oligomer formation was not apparent until 24 weeks of age and appeared by 36 weeks of age when it appeared to be associated with neuronal processes. (C) Plaques were present by 36 weeks of age, but not earlier (quantified in F). (D and G) A dot plot quantification with the Aβ-oligomer specific antibody, A11, revealed increases in Aβ oligomers through aging in the hAPP-J20 mouse, with a significant increase in 36-week-old hAPP-J20 mice. (H) Quantification of Aβ by ELISA revealed an increase in total Aβ from 6 (p<0.05) and 12 (p<0.05) to 36 weeks of age in the hAPP-J20 mouse. Each value represents the mean ± standard error of the mean (SEM). *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001.</p
Hippocampal-dependent memory deficits are observed in 13–15 month old hAPP mice.
No full text<p>A, Performance in the acquisition portion of the Morris water maze. In the cued platform portion, 2-way repeated measures ANOVA indicates an overall difference between NTG and hAPP mice (p<0.01). Asterisk denotes p<0.05 for individual data points. There was also a significant difference between NTG and hAPP mice in the hidden platform portion of the water maze, although no individual point reached significance in post-hoc tests (2-way repeated measures ANOVA p<0.01). B–C, During the probe trial test for memory that occurred 24 hrs after the last training trial of the hidden platform acquisition phase, NTG mice spent more time in the target quandrant relative to the other three quadrants (B) whereas hAPP mice did not (C). D, The latency for hAPP mice to reach the correct quadrant for the first time during the probe trial was higher than that for NTG mice. E, Representative paths swum during the probe trial for a NTG and an hAPP mouse. F, Swim speed was lower for hAPP mice than NTG mice in the cued portion of the water maze, but was similar to NTG mice during the hidden platform portion of the maze. Swim speeds were compared by assessing the average swim speeds over all sessions in the cued or hidden platform portions of the test. n = 7–11/genotype. T, target; AR, adjacent right; AL, adjacent left; OP, opposite. *p<0.05, **p<0.01.</p
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