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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: Decoding the synaptic dysfunction of bioactive human AD brain soluble Aβ to inspire novel therapeutic avenues for Alzheimer’s disease

Fig. 5

Soluble Aβ peptides with longer C-termini confer greater synaptic toxicity. (a) The short Aβ1–37 synthetic peptide did not impair hippocampal LTP at concentrations of 200 nM (red, n = 7, p > 0.05), while the same dose of the longer Aβ1–42 peptide showed significant inhibition (blue, n = 6, p < 0.001); (b) N-terminally truncated synthetic Aβ1–16 and Aβ17–42 effect on the hippocampal LTP. (c) Summary data of LTP effects of Aβ peptides of increasing lengths at 200 nM concentrations; (d) The whole 7PA2 CM as well as immunoprecipitated NTE-Aβs (black open circles, n = 7, p < 0.001) and the CM remaining CM after depletion of APPs by DE23 resin (red circles, n = 7, p < 0.001) all inhibit LTP, while the isolated APPs alone (blue diamonds, n = 7, p > 0.05) does not; (e) Treatment of slices with synthetic pre-Aβ (− 30 to − 1) does not facilitate synthetic Aβ1–40 to induce synaptotoxicity, that is to say, a synthetic APP-34 to − 1 fragment added to an Aβ1–40 peptide does not inhibit LTP (n = 6, p > 0.05); (f) Summary data of synthetic peptides containing or not various lengths (− 10. -20, − 30) of APP prior to the Aβ1–40 Asp1 start site (called “preAβ”) and N-terminal extension on Aβ1–40 do not inhibit LTP. (n = 6~ 8). *: p < 0.05; **: p < 0.01

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