Abstract

Objectives Retina abnormalities are related to cognitive disorders in patients with Alzheimer's disease (AD). Retinal amyloid beta (Aβ) can be labeled by curcumin. We measured Aβ content in the cerebrum and retina of APPswe/PS1dE9 (APP) transgenic mice with early age to investigate the correlation between cerebrum and retina. Methods APP mice and age-matched wild-type mice were investigated every month from age 2 months to 6 months to assess changes in Aβ content in the retina and cerebrum. At the beginning of each month, mice were fed a curcumin diet (50 mg/kg/day) for 7 consecutive days. The Aβ levels in the retina and cerebrum were measured by ELISAs. Correlations were identified between retinal and cerebral Aβ contents using Pearson's correlation. Results In the absence of curcumin, there was a significant correlation between Aβ contents in the retina and cerebrum of APP mice (r = 0.7291, P = 0.0014). With increasing age, Aβ-mediated degenerative change in the cerebrum (P < 0.001 in 5 months) and retina (P < 0.01 in 5 months) increased significantly. The inhibitory effect of curcumin on the Aβ level was significant in the cerebrum (P < 0.001) and retina (P < 0.01) of older APP mice in the early stage of life. Conclusion We observed a significant correlation between the Aβ content in the retina and Aβ content in the cerebrum of APP mice. Our data suggest an appropriate time to measure retinal Aβ. Although curcumin can label Aβ in the retina, it also suppresses Aβ levels and weakens the degree of correlation between Aβ in cerebrum and retina tissues.

Highlights

  • Diagnosis of Alzheimer’s disease (AD) is essential for treatment [1]

  • At 5 months of age, curcumin had a significant effect on the Aβ content

  • Aβ content was significantly higher in the APPN group compared with that in the WTN group (P < 0:05 from 3 month to 6 month)

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Summary

Introduction

Diagnosis of Alzheimer’s disease (AD) is essential for treatment [1]. Most diagnostic methods for AD are based on clinical symptoms [2]. People in the presymptomatic stage of AD have no clinical symptoms (including impairment in episodic memory). “Amyloid beta” (Aβ), which denotes peptides of 36-43 amino acids, is a major pathologic hallmark in the central nervous system (CNS) of patients with AD [3, 4]. Amyloidal precursor protein (APP) is first cleaved by the enzymes βsecretase and γ-secretase and released into the space between cells [5]. Soluble Aβ oligomers are more toxic than deposited plaques [6]. Aβ plaques are found in the brains of many elderly people without

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