Chebulinic and Gallic Acid Treat Novel Targets in Alzheimer's Disease

Overview

Alzheimer's Disease (AD), a neurodegenerative disorder affecting millions yearly, remains a leading cause of death with no cure. Previous studies have conflicted over the impact of amyloid beta (Aβ) peptides on molecules including Matrix Metalloproteinase-9 (MMP-9), brain-derived neurotrophic factor (BDNF), and CD44. This study examines the effects of Aβ 1-40 on the expressions of MMP-9, BDNF, and Hyaluronidase-1 (HYAL-1), a protein that interacts with CD44. The study also examines chebulinic acid (ChA) and gallic acid (GA) as potential treatments against Aβ. Cell adhesion, caspase, and ELISA assays assessed the effects of Aβ, ChA, and GA on inflammation, apoptosis, and protein expression in neuronal and immune cells. Aβ increased cell attachment, with ChA and GA reversing the effect. Furthermore, ChA and GA counteracted the increased caspase activity caused by Aβ. Aβ decreased MMP-9 and BDNF amounts, with ChA and GA mitigating the impact. In addition, Aβ increased HYAL-1 expression in neurons, identifying HYAL-1 as a novel target for AD progression. ChA also counteracted Aβ’s effects on HYAL-1. This study supported previous studies that found MMP-9 and BDNF downregulation by Aβ and identified HYAL-1 as a novel target for further examination of AD, also indicating ChA and GA as potential treatment options.

Competition history

• AJAS 2025 Category not listed

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