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Lentivirus-mediated expression of human secreted amyloid precursor protein-alpha prevents development of memory and plasticity deficits in a mouse model of Alzheimer’s disease.

Tan, Valerie T. Y., Mockett, Bruce G., Ohline, Shane M., Parfitt, Karen D., Wicky, Hollie E., Peppercorn, Katie, Schoderboeck, Lucia, Yahaya, Mohamad Fairuz bin, Tate, Warren P., Hughes, Stephanie M., Abraham, Wickliffe C.·2018·Molecular Brain
DOI 10.1186/s13041-018-0348-9PMC PMC5806250
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Fig. 1 In vitro and in vivo lentiviral transduction of hippocampal neurons with sAPPα-copGFP. a The transduction marker copGFP (green) was expressed in mouse primary hippocampal neurons co-labelled with the neuronal marker MAP2 (red) and the nuclear marker DAPI (blue). Scale bar, 50 μm. b Detection of sAPPα in media from primary mouse neural cultures transduced with LV-sAPPα, but not LV-control. The right-hand lane of the western blot illustrates the band from a sample fortified with purified sAPPα [22]. c-e Examples of in vivo copGFP expression (green) showing transduction of hippocampal regions containing LV-transduced neurons in slices from wild-type (c), transgenic-control (d) and transgenic-sAPPα (e) mice. Scale bar: 1 mm
Fig. 1 In vitro and in vivo lentiviral transduction of hippocampal neurons with sAPPα-copGFP. a The transduction marker copGFP (green) was expressed in mouse primary hippocampal neurons co-labelled with the neuronal marker MAP2 (red) and the nuclear marker DAPI (blue). Scale bar, 50 μm. b Detection of sAPPα in media from primary mouse neural cultures transduced with LV-sAPPα, but not LV-control. The right-hand lane of the western blot illustrates the band from a sample fortified with purified sAPPα [22]. c-e Examples of in vivo copGFP expression (green) showing transduction of hippocampal regions containing LV-transduced neurons in slices from wild-type (c), transgenic-control (d) and transgenic-sAPPα (e) mice. Scale bar: 1 mmCC BY · PubMed Central
Fig. 2 sAPPα transduction rescued spatial learning and memory in the APP/PS1 mice. a In the open field all groups preferred the periphery (p < 0.001), but this preference was stronger in Tg-controls (n = 11) compared to WT-control (n = 22, p < 0.05, Students t-test). The Tg-sAPPa group showed a trend toward reduced time in the periphery (n = 23, p = 0.084) compared to Tg-controls. b Mean distances travelled by each group were not significantly different. c For spatial reference memory acquisition in the water maze, there was a significant group main effect (F(1,54) = 3.33, p = 0.043) for proximity to the platform, with a strong trend for Tg-controls to be impaired relative to WT-control animals (Tukey p = 0.071), while Tg-sAPPα animals performed significantly better than Tg-control animals (p = 0.046). d There was a significant group main effect (F(1,54) = 3.33, p = 0.043) with a strong trend for impaired performance on day 6 by the Tg-control group compared to WT-controls (p = 0.068) and by enhanced performance of the Tg-sAPPα group compared to Tg-controls (p = 0.018). e, f Tg-control mice had significantly poorer memory for the platform position than WT-controls (Probe 1: proximity p = 0.004, crossings p = 0.037; Probe 2: proximity p = 0.016, crossings p = 0.006). Tg-sAPPα mice exhibited a partial rescue in Probe 1 and a complete rescue in Probe 2 (proximity p = 0.022, crossings p = 0.006 compared to Tg-control). g, h Spatial working memory testing revealed a significant group main effect (G, Day 2: p < 0.001; H, Day 3: p = 0.004). On both days, Tg-controls performed significantly worse than WT-controls (Day 1: p = 0.025; Day 2: p = 0.034) while Tg-sAPPα animals were significantly better than Tg-controls (Day 1: p < 0.001; Day 2: p = 0.003). *p < 0.05, **p < 0.01, ***p < 0.001
Fig. 2 sAPPα transduction rescued spatial learning and memory in the APP/PS1 mice. a In the open field all groups preferred the periphery (p < 0.001), but this preference was stronger in Tg-controls (n = 11) compared to WT-control (n = 22, p < 0.05, Students t-test). The Tg-sAPPa group showed a trend toward reduced time in the periphery (n = 23, p = 0.084) compared to Tg-controls. b Mean distances travelled by each group were not significantly different. c For spatial reference memory acquisition in the water maze, there was a significant group main effect (F(1,54) = 3.33, p = 0.043) for proximity to the platform, with a strong trend for Tg-controls to be impaired relative to WT-control animals (Tukey p = 0.071), while Tg-sAPPα animals performed significantly better than Tg-control animals (p = 0.046). d There was a significant group main effect (F(1,54) = 3.33, p = 0.043) with a strong trend for impaired performance on day 6 by the Tg-control group compared to WT-controls (p = 0.068) and by enhanced performance of the Tg-sAPPα group compared to Tg-controls (p = 0.018). e, f Tg-control mice had significantly poorer memory for the platform position than WT-controls (Probe 1: proximity p = 0.004, crossings p = 0.037; Probe 2: proximity p = 0.016, crossings p = 0.006). Tg-sAPPα mice exhibited a partial rescue in Probe 1 and a complete rescue in Probe 2 (proximity p = 0.022, crossings p = 0.006 compared to Tg-control). g, h Spatial working memory testing revealed a significant group main effect (G, Day 2: p < 0.001; H, Day 3: p = 0.004). On both days, Tg-controls performed significantly worse than WT-controls (Day 1: p = 0.025; Day 2: p = 0.034) while Tg-sAPPα animals were significantly better than Tg-controls (Day 1: p < 0.001; Day 2: p = 0.003). *p < 0.05, **p < 0.01, ***p < 0.001CC BY · PubMed Central
Fig. 3 Expression of sAPPα partially restored hippocampal LTP in transgenic mice. a, b There were no significant genotype or treatment effects on the I/O curves in CA1 for either the (a) EPSP slope, (p = 0.17 and 0.14, respectively) or (b) population spike amplitude (p = 0.14 and 0.63, respectively, indicating that basal synaptic transmission and cell excitability were unaffected in Tg mice and sAPPα over-expression. c There were no group differences in paired-pulse facilitation of the fEPSP (WT-control: n = 22; Tg-control: n = 12; Tg-sAPPα: n = 17, F(2,48) = 0.32, p = 0.73), nor a group x interval interaction (F(2,48) = 0.96, p = 0.39), indicating no difference in basal transmitter release probability. (d) Paired-pulse inhibition was reduced in Tg-controls compared to WT-controls (WT-control: n = 16; Tg-control: n = 10; F(2,38) = 4.18, p = 0.023), indicating an impairment of recurrent inhibition. A partial rescue was produced by sAPPα expression. (e, f) TBS delivered to the Schaffer collaterals induced robust potentiation in all groups but which decayed at different rates between groups. Significant group differences were observed at both 1 h (F(2,49) = 4.20, p = 0.021) and 2 h post-TBS (F(2,49) = 5.44, p = 0.007) with Tg-controls significantly impaired (26.1 ± 6.9%, n = 11) compared to WT-controls (51.9 ± 7.4%, n = 21; p < 0.05) after 1 h. LTP in the Tg-sAPPα indicating a partial recovery of LTP expression. The partial recovery was still observed 2 h post-TBS (WT-controls: 36.8 ± 7.5%, n = 21; Tg-controls: 9.7 ± 6.2%, n = 11; Tg-sAPPα: 22.5 ± 3.5%, n = 18). *p < 0.05
Fig. 3 Expression of sAPPα partially restored hippocampal LTP in transgenic mice. a, b There were no significant genotype or treatment effects on the I/O curves in CA1 for either the (a) EPSP slope, (p = 0.17 and 0.14, respectively) or (b) population spike amplitude (p = 0.14 and 0.63, respectively, indicating that basal synaptic transmission and cell excitability were unaffected in Tg mice and sAPPα over-expression. c There were no group differences in paired-pulse facilitation of the fEPSP (WT-control: n = 22; Tg-control: n = 12; Tg-sAPPα: n = 17, F(2,48) = 0.32, p = 0.73), nor a group x interval interaction (F(2,48) = 0.96, p = 0.39), indicating no difference in basal transmitter release probability. (d) Paired-pulse inhibition was reduced in Tg-controls compared to WT-controls (WT-control: n = 16; Tg-control: n = 10; F(2,38) = 4.18, p = 0.023), indicating an impairment of recurrent inhibition. A partial rescue was produced by sAPPα expression. (e, f) TBS delivered to the Schaffer collaterals induced robust potentiation in all groups but which decayed at different rates between groups. Significant group differences were observed at both 1 h (F(2,49) = 4.20, p = 0.021) and 2 h post-TBS (F(2,49) = 5.44, p = 0.007) with Tg-controls significantly impaired (26.1 ± 6.9%, n = 11) compared to WT-controls (51.9 ± 7.4%, n = 21; p < 0.05) after 1 h. LTP in the Tg-sAPPα indicating a partial recovery of LTP expression. The partial recovery was still observed 2 h post-TBS (WT-controls: 36.8 ± 7.5%, n = 21; Tg-controls: 9.7 ± 6.2%, n = 11; Tg-sAPPα: 22.5 ± 3.5%, n = 18). *p < 0.05CC BY · PubMed Central
Fig. 4 Effect of sAPPα expression on the development of amyloid pathology. a-c Congo red staining of coronal brain sections from (a) WT-control, (b) Tg-sAPPα and (c) Tg-control animals revealed an absence of amyloid plaques in WT-control brains, but extensive plaque formation in Tg-sAPPα and Tg-control brains. d-e No significant differences in plaque density were observed between Tg- sAPPα and Tg-control in the hippocampus (p = 0.316, d) or overlying neocortex (p = 0.297, E). f-i Human amyloid-β load in the hippocampus. f Soluble Aβ1–40 levels differed between groups (one-way ANOVA F(2,27) = 17.40, p < 0.001), with higher levels in in Tg-control animals compared to wildtypes (WT-control: 15.6 ± 1.6 ng/mg, n = 12; Tg-control: 50.7 ± 6.9 ng/mg, n = 6, post-hoc Tukey p = 0.001), but no effect of sAPPα treatment compared to Tg-control (Tg-sAPPα: 56.1 ± 7.1 ng/mg, n = 12, Tukey = 0.820). g Insoluble Aβ1–40 levels showed a significant overall group effect (F(2,28 = 10.70) and while there was no significant difference between WT-control and Tg-control (WT-control, 2.8 ± 0.3 ng/mg, n = 13, Tg-control, 5.5 ± 1.0 ng/mg, n = 6, Tukey p = 0.145), the levels were elevated in the Tg-sAPPα group compared to WT-control (Tg-sAPPα 7.9 ± 1.1 ng/mg, Tukey p < 0.001) and they were not different to Tg-control (Tukey p + 0.194). (H) Soluble Aβ1–42 levels did not show any differences between groups. i For the insoluble fraction, there was an overall group effect (F(2,28) = 20.47, p < 0.001, whereby Tg-controls showed the expected greater Aβ1–42 load (2.26 ± 0.46 ng/mg, n = 6) compared to WT-controls (0.31 ± 0.077 ng/mg, n = 13; Tukey p = 0.006) and this level was not significantly affected by sAPPα over-expression (3.25 ± 0.48 ng/mg, n = 12, Tukey p = 0.220). **p < 0.01, ***p < 0.001, Scale bar: 1 mm
Fig. 4 Effect of sAPPα expression on the development of amyloid pathology. a-c Congo red staining of coronal brain sections from (a) WT-control, (b) Tg-sAPPα and (c) Tg-control animals revealed an absence of amyloid plaques in WT-control brains, but extensive plaque formation in Tg-sAPPα and Tg-control brains. d-e No significant differences in plaque density were observed between Tg- sAPPα and Tg-control in the hippocampus (p = 0.316, d) or overlying neocortex (p = 0.297, E). f-i Human amyloid-β load in the hippocampus. f Soluble Aβ1–40 levels differed between groups (one-way ANOVA F(2,27) = 17.40, p < 0.001), with higher levels in in Tg-control animals compared to wildtypes (WT-control: 15.6 ± 1.6 ng/mg, n = 12; Tg-control: 50.7 ± 6.9 ng/mg, n = 6, post-hoc Tukey p = 0.001), but no effect of sAPPα treatment compared to Tg-control (Tg-sAPPα: 56.1 ± 7.1 ng/mg, n = 12, Tukey = 0.820). g Insoluble Aβ1–40 levels showed a significant overall group effect (F(2,28 = 10.70) and while there was no significant difference between WT-control and Tg-control (WT-control, 2.8 ± 0.3 ng/mg, n = 13, Tg-control, 5.5 ± 1.0 ng/mg, n = 6, Tukey p = 0.145), the levels were elevated in the Tg-sAPPα group compared to WT-control (Tg-sAPPα 7.9 ± 1.1 ng/mg, Tukey p < 0.001) and they were not different to Tg-control (Tukey p + 0.194). (H) Soluble Aβ1–42 levels did not show any differences between groups. i For the insoluble fraction, there was an overall group effect (F(2,28) = 20.47, p < 0.001, whereby Tg-controls showed the expected greater Aβ1–42 load (2.26 ± 0.46 ng/mg, n = 6) compared to WT-controls (0.31 ± 0.077 ng/mg, n = 13; Tukey p = 0.006) and this level was not significantly affected by sAPPα over-expression (3.25 ± 0.48 ng/mg, n = 12, Tukey p = 0.220). **p < 0.01, ***p < 0.001, Scale bar: 1 mmCC BY · PubMed Central
Fig. 5 Cellular markers for neuronal and non-neuronal cells. a Western blot analysis of the microglial marker Iba-1 (insoluble fraction), normalised to WT-control, showed an overall group effect (one-way ANOVA F(2,28) = p = 0.041) with a trend toward higher levels in Tg mice (WT-control: 1.0 ± 0.083, n = 12; Tg-control: 1.37 ± 0.299, n = 6), that was even more evident in the Tg-sAPPα group (Tg-sAPPα: 1.39 ± 0.065, n = 13; post-hoc Tukey p = 0.046). b GFAP levels (insoluble fraction) showed a significant overall group effect (F(2,27) = 10.92, p < 0.001), whereby there was significantly higher levels in the Tg-control group compared to the WT-control group (WT-control: 0.998 ± 0.105, n = 13; Tg-control: 1.81 ± 0.284, n = 6, Tukey p = 0.007) and expression of sAPPα did not alter this higher expression level (Tg-sAPPα: 1.86 ± 0.23, n = 11, Tukey p = 0.974). c Neither genotype (WT-control: 1 ± 0.02, n = 13; Tg-control: 1.07 ± 0.674, n = 6) nor sAPPα treatment (Tg-sAPPα: 0.96 ± 0.043, n = 12) affected the presynaptic marker synaptophysin (soluble fraction). d Levels of the postsynaptic marker PSD-95 (insoluble fraction) were also not affected by the APP/PS1 genotype (WT-control: 1.00 ± 0.072, n = 13; Tg-control: 0.82 ± 0.086, n = 5), although the PSD-95 levels tended to be higher for the Tg-sAPPα group compared to Tg-controls (Tg- sAPPα: 1.066 ± 0.082, n = 12, t(17) = − 1.90, p = 0.074. Representative western blots are presented. Note that in the case of Iba-1, its illustration and that of tubulin are from the same blot, but at different exposures. Tubulin was used as the loading control. *p < 0.05, **p < 0.01; synapto: synaptophysin; Lane labels: WT, WT-control; Tg, Tg-control; TgS, Tg-sAPPα
Fig. 5 Cellular markers for neuronal and non-neuronal cells. a Western blot analysis of the microglial marker Iba-1 (insoluble fraction), normalised to WT-control, showed an overall group effect (one-way ANOVA F(2,28) = p = 0.041) with a trend toward higher levels in Tg mice (WT-control: 1.0 ± 0.083, n = 12; Tg-control: 1.37 ± 0.299, n = 6), that was even more evident in the Tg-sAPPα group (Tg-sAPPα: 1.39 ± 0.065, n = 13; post-hoc Tukey p = 0.046). b GFAP levels (insoluble fraction) showed a significant overall group effect (F(2,27) = 10.92, p < 0.001), whereby there was significantly higher levels in the Tg-control group compared to the WT-control group (WT-control: 0.998 ± 0.105, n = 13; Tg-control: 1.81 ± 0.284, n = 6, Tukey p = 0.007) and expression of sAPPα did not alter this higher expression level (Tg-sAPPα: 1.86 ± 0.23, n = 11, Tukey p = 0.974). c Neither genotype (WT-control: 1 ± 0.02, n = 13; Tg-control: 1.07 ± 0.674, n = 6) nor sAPPα treatment (Tg-sAPPα: 0.96 ± 0.043, n = 12) affected the presynaptic marker synaptophysin (soluble fraction). d Levels of the postsynaptic marker PSD-95 (insoluble fraction) were also not affected by the APP/PS1 genotype (WT-control: 1.00 ± 0.072, n = 13; Tg-control: 0.82 ± 0.086, n = 5), although the PSD-95 levels tended to be higher for the Tg-sAPPα group compared to Tg-controls (Tg- sAPPα: 1.066 ± 0.082, n = 12, t(17) = − 1.90, p = 0.074. Representative western blots are presented. Note that in the case of Iba-1, its illustration and that of tubulin are from the same blot, but at different exposures. Tubulin was used as the loading control. *p < 0.05, **p < 0.01; synapto: synaptophysin; Lane labels: WT, WT-control; Tg, Tg-control; TgS, Tg-sAPPαCC BY · PubMed Central
Fig. 6 Delivery of sAPPα, either in vivo or in vitro, after plaque development, completely rescued the impaired LTP in Tg-controls. a Chronically administered sAPPα by lentivirus-mediated expression in adult (10 months) Tg mice completely rescued the deficit in hippocampal LTP, measured 3 months after viral transduction (at 13 months of age). LTP measured 60 min after TBS (arrow) revealed a significant deficit in LTP expression in Tg-control mice compared to WT-controls (WT-controls: 71.1 ± 6.7%, n = 11; Tg-controls 36.3 ± 10.0%, n = 9; p = 0.008). This deficit was completely rescued by sAPPα over-expression (Tg-sAPPα: 72.2 ± 2.4%, n = 12; p = 0.008 compared to Tg-controls). b LTP induced in hippocampal slices from aged Tg mice (18–20 months of age), was impaired compared to WT-controls when measured 60 min post-TBS (WT-control: 67.2 ± 7.5%, n = 9; Tg-control: 29.4 ± 4.7%, n = 7; p = 0.002). LTP expression was again completely rescued by acutely applied recombinant human sAPPα (10 nM) beginning 30 min before delivery of the TBS (Tg-sAPPα: 73.7 ± 16.7%, n = 10; p = 0.737 compared to WT-controls, p = 0.048 compared to Tg-controls). No effect of sAPPα on WT-control LTP was observed (WT-sAPPα: 62.1 ± 9.4%, n = 6; p = 0.684)
Fig. 6 Delivery of sAPPα, either in vivo or in vitro, after plaque development, completely rescued the impaired LTP in Tg-controls. a Chronically administered sAPPα by lentivirus-mediated expression in adult (10 months) Tg mice completely rescued the deficit in hippocampal LTP, measured 3 months after viral transduction (at 13 months of age). LTP measured 60 min after TBS (arrow) revealed a significant deficit in LTP expression in Tg-control mice compared to WT-controls (WT-controls: 71.1 ± 6.7%, n = 11; Tg-controls 36.3 ± 10.0%, n = 9; p = 0.008). This deficit was completely rescued by sAPPα over-expression (Tg-sAPPα: 72.2 ± 2.4%, n = 12; p = 0.008 compared to Tg-controls). b LTP induced in hippocampal slices from aged Tg mice (18–20 months of age), was impaired compared to WT-controls when measured 60 min post-TBS (WT-control: 67.2 ± 7.5%, n = 9; Tg-control: 29.4 ± 4.7%, n = 7; p = 0.002). LTP expression was again completely rescued by acutely applied recombinant human sAPPα (10 nM) beginning 30 min before delivery of the TBS (Tg-sAPPα: 73.7 ± 16.7%, n = 10; p = 0.737 compared to WT-controls, p = 0.048 compared to Tg-controls). No effect of sAPPα on WT-control LTP was observed (WT-sAPPα: 62.1 ± 9.4%, n = 6; p = 0.684)CC BY · PubMed Central

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Cited by

Sorted by citations

Metadata

Authors
Tan, V. T. Y., Mockett, B. G., Ohline, S. M., Parfitt, K. D., Wicky, H. E., Peppercorn, K., Schoderboeck, L., Yahaya, M. F. B., Tate, W. P., Hughes, S. M., & Abraham, W. C.
ORCID
Abraham, Wickliffe C.
Venue
Molecular Brain
Publisher
Springer Science and Business Media LLC
Published
2018-02-09
Volume
11
Issue
1
ISSN
1756-6606
DOI
10.1186/s13041-018-0348-9
PMC
PMC5806250
Cited by
61
References
5
Language
en
Funders
  • Health Research Council of New Zealand (10-170)
  • Ministry of Higher Education, Malaysia

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

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