Abstract
Glucose excursions in type 2 diabetes modulate amyloid-related proteins associated with dementia
Highlights
A case-controlled study was undertaken, enrolling type 2 diabetes (T2D) and control subjects
APP was elevated at baseline (p < 0.01), and SNCA (p < 0.01) and ApoB (p < 0.05) decreased, in T2D whilst there was no difference between controls and T2D subjects at baseline for the other Alzheimer’s disease (AD)-related proteins
The T2D cohort had higher circulating APP and lower SNCA; these results accorded with the findings in a previous report detailing circulating protein levels in AD [1]: accumulations of β-amyloid (Aβ) and tau proteins in the brain are pathognomonic of AD, and these deposits are believed to be a central facet in the pathophysiology of developing AD
Summary
A case-controlled study was undertaken, enrolling type 2 diabetes (T2D) and control subjects. APP was elevated at baseline (p < 0.01), and SNCA (p < 0.01) and ApoB (p < 0.05) decreased, in T2D whilst there was no difference between controls and T2D subjects at baseline for the other AD-related proteins. APOA1 and C3 were significantly reduced (p = 0.05). The T2D cohort had higher circulating APP and lower SNCA; these results accorded with the findings in a previous report detailing circulating protein levels in AD [1]: accumulations of β-amyloid (Aβ) and tau proteins in the brain are pathognomonic of AD, and these deposits are believed to be a central facet in the pathophysiology of developing AD.
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