Figure 7: ILEI overexpression ameliorates the memory deficit and reduces brain Aβ burden in APP-Tg mice. | Nature Communications

Figure 7: ILEI overexpression ameliorates the memory deficit and reduces brain Aβ burden in APP-Tg mice.

From: The FAM3 superfamily member ILEI ameliorates Alzheimer’s disease-like pathology by destabilizing the penultimate amyloid-β precursor

Figure 7

(a) Spontaneous alternation in the Y-maze test. APP-Tg (3 females at 6 months age, 6 males and 6 females at 12 months age), ILEI-Tg (5 males and 4 females at 12 months age), APP/ILEI-Tg (3 females at 6 months age, 5 males and 6 females at 12 months age) and non-Tg (5 males and 4 females at 12 months age) littermate mice were used. Data are expressed as percentage (mean±s.e.m.). **P<0.01, NS, not significant by Student’s t-test. (b) Immunostaining images with anti-ILEI antibody (top) and anti-Aβ antibody (bottom) using serial brain sections from 12-month-old APP-Tg (left) and APP/ILEI-Tg (right) mice. Scale bars, 200 μm. (c–f) Aβ burden in brains of APP-Tg and APP/ILEI-Tg mice (12 months old, n=6 per genotype). The plaque number (c) and the area occupied by plaques (d) in Aβ-immunostained sections of prefrontal cortex (grey bars) and hippocampus (white bars) (mean±s.e.m.). The relative levels of Aβ40 (black bars) and Aβ42 (grey bars) in soluble (e) and insoluble (f) fractions (mean±s.e.m.). **P<0.01 versus the APP-Tg by Student’s t-test. Aβ concentrations were as follows: soluble Aβ40 of APP-Tg, 19.79±2.66; soluble Aβ42 of APP-Tg, 4.69±0.72; insoluble Aβ40 of APP-Tg, 1362.56±152.88; insoluble Aβ42 of APP-Tg, 517.80±57.82; soluble Aβ40 of APP/ILEI-Tg, 8.14±1.21; soluble Aβ42 of APP/ILEI-Tg, 1.95±0.42; insoluble Aβ40 of APP/ILEI-Tg, 788.68±142.23; insoluble Aβ42 of APP/ILEI-Tg, 312.92±38.80 pmol per g protein (mean±s.e.m.).

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