Figure 4. Anchorless soluble PrP^C reduces hippocampal LTP impairment in APPPS1⁺ mice.

1. Percentage of strain-specific microsatellites in APPPS1⁺tg44^tg/−Prnp^−/o (n = 5) and APPPS1⁺tg44^−/−Prnp^−/o (n = 5) mice is displayed by box plot. No significant difference in the genetic background was detected (Mann–Whitney U-test, two-tailed, p > 0.05).
2. LTP was induced in slices prepared from 4-month-old tg44^tg/−Prnp^−/o (n = 5) and tg44^−/−Prnp^−/o (n = 7) mice, but was impaired in slices from APPPS1⁺tg44^−/−Prnp^−/o mice (n = 6) and partially rescued in APPPS1⁺tg44^tg/−Prnp^−/o (n = 7) mice. Basal synaptic transmission was normal as indicated by normal input–output curve (stimulus intensity vs. fEPSP slope). All mice were compound heterozygotes for the ‘Zurich-I’ (Prnp^o) and the ‘Edbg’ (Prnp⁻) knockout alleles of Prnp.
3. APP expression and processing by secretases were similar in APPPS1⁺tg44^tg/−Prnp^−/o and APPPS1⁺tg44^−/−Prnp^−/o mice at 4 months of age. Left panel: representative SDS–PAGE followed by immunoblotting using an APP C-terminal antibody detecting full-length APP and C-terminal fragments (αβ-CTF); actin was used as loading control. Right panel: quantitation of chemiluminescence revealed no difference in APP, α-CTF and β-CTF between the two groups.
4. TRIS-soluble (left panel), detergent-soluble (middle panel) and insoluble (right panel) human Aβ₄₂ levels as assessed by ELISA. Each symbol denotes one individual mouse.