Table 1.
Demographic information for study participants.
Figure 1.
Plasma levels of total sAPP in control and autistic patients.
Plasma levels of total sAPP (α and β) were assayed by Western blot from control and autistic patients. Autistic patients were classified as mild-to-moderate or severe based on clinical CARS score. Total sAPP bands were analyzed by scanning the final blot followed by densitometry, ImageJ quantification, and normalization against β-actin bands. Statistical significance was assessed using ANOVA. No significant differences observed in mean total sAPP levels between control or autistic patients.
Figure 2.
Plasma levels of sAPPα and sAPPβ in control and autistic patients.
(A) Plasma sAPPα and (B) sAPPβ levels were quantified from albumin-depleted samples of control and autistic patients by corresponding ELISA procedures. sAPPα and sAPPβ quantities were normalized against immunodepleted plasma protein concentrations. No difference was observed in the mean plasma sAPPα and sAPPβ levels of mild-to-moderate cases of autism relative to controls. Plasma sAPPα levels were significantly increased and sAPPβ levels decreased in severely autistic patients relative to controls Statistical significance assessed using ANOVA followed by post-hoc Dunnett's t-test for multiple comparisons (*p<0.05).
Figure 3.
Plasma levels of Aβ1-40 and Aβ1-42 in control and autistic patients.
(A) Aβ1-40 levels were quantified by a specific sandwich ELISA in plasma samples. Aβ1-40 quantities were normalized against plasma protein concentrations. Statistical significance was assessed by ANOVA. Plasma Aβ1-40 levels are significantly decreased in severely autistic patients relative to controls (*p = 0.031). (B) Aβ1-42 levels were quantified by ELISA in non-immunodepleted plasma samples. Absolute Aβ1-42 quantities were normalized against plasma protein concentrations. Statistical significance was assessed by ANOVA. Plasma Aβ1-42 levels are significantly different among all groups as analyzed by ANOVA. Differences in levels between severely autistic patients and normal controls are nearly significant (p = 0.055). (C) Ratios of Aβ1-40 and Aβ1-42 were calculated. No significant differences were observed between any groups (p = 0.56).
Figure 4.
Plasma Aβ levels normalized to sAPPα.
To better characterize the balance between amyloidogenic and non-amyloidogenic pathways in autism, ratios of (A) Aβ1-40:sAPPα and (B) Aβ1-42:sAPPα were calculated for each patient. Both ratios were significantly reduced following ANOVA and post-hoc Dunnett's multiple comparison test. *p = 0.003, +p = 0.012.
Figure 5.
Plasma levels of BDNF in control and autistic patients.
BDNF levels were quantified by ELISA in plasma samples from control and autistic patients. Absolute quantities were normalized against plasma protein concentrations. (A) Mean BDNF levels are significantly reduced in severely autistic patients compared to controls when adjusting age as a covariate and following post-hoc Sidak's adjustment for multiple comparisons. (B) Estimated marginal means for plasma BDNF levels were computed with the age covariate held at 86.18 months. The mean difference between control and severely autistic patients is enhanced when age is regressed (*p = 0.038). Thus, BDNF levels are decreased in the plasma of severely autistic patients relative to controls.