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Therapeutic potential of coffee-derived exosome-like nanoparticles in an experimental Aβ1–42-induced Alzheimer's disease model: evidence from FDG-PET imaging and Tau/APP expression

biochemistry
geriatrics
neurology
pathology

Abstract

Background. Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta 1–42 (Aβ1–42) accumulation, tau pathology, and metabolic dysfunction. This study investigated the therapeutic potential of coffee-derived exosome-like nanoparticles (CELNs) in an experimental Aβ1–42-induced AD rat model.

Methods. Fifty male Sprague–Dawley rats were randomly divided into five groups (n = 10 each): Control (C), sham (SF), AD, AD treated with a low dose of CELNs (AD + LE, 10 mg/kg/day), and AD treated with a high dose of CELNs (AD + HE, 20 mg/kg/day) for 14 days. CELNs were quantified and characterized using the bicinchoninic acid method, scanning electron microscopy, and nanoparticle tracking analysis (NTA). Micropet/CT FDG imaging of the central nervous system was performed in all groups at the end of treatment. Subsequently, all animals were sacrificed, and hippocampal tissues were subjected to histopathological analysis.

Results. Micropet imaging demonstrated a significant, dose-dependent increase in cerebral glucose metabolism in AD rats treated with CELNs compared with the untreated AD group. Histopathological evaluations were consistent with the imaging data: in AD groups receiving CELNs, phospho-tau and beta-amyloid precursor protein expression were significantly reduced in the hippocampal CA2 and dentate gyrus regions in a dose-dependent manner.

Conclusions. These findings indicate that CELNs may restore metabolic function and reduce AD-related neuropathology in this experimental model. CELNs represent promising therapeutic candidates for AD.

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