AI Article Synopsis
- Alzheimer's disease (AD) is marked by memory loss and cognitive decline, linked to amyloid beta and TAU protein problems.
- A study tested the effects of cucurbitacin E (CuE) on TAU fibril formation in rats with AD induced by okadaic acid.
- Results indicate that CuE may improve memory by decreasing TAU accumulation, suggesting it deserves further research for potential therapeutic use.
Article Abstract
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive memory loss and cognitive decline, with hallmark pathologies related to amyloid beta (Aβ) and TAU. Natural phytochemicals show promise for drug discovery to fill the current therapeutic innovation gap in AD. This study investigated the effect of cucurbitacin E (CuE), one of the bioactive components of , on TAU fibril formation in okadaic acid-induced AD in rats. In a randomized design, we assigned 30 female rats to one of five experimental groups: (1) control, (2) stereotaxic surgery, (3) stereotaxic surgery + artificial cerebrospinal fluid, (4) stereotaxic surgery + okadaic acid (AD model), and (5) stereotaxic surgery + okadaic acid + CuE treatment. For experimental groups 4 and 5, rats were administered OKA-ICV (200 ng/kg) followed by CuE (4 mg/[kg·day], intraperitoneally) for 20 days. Expression of the and genes associated with TAU metabolism, hippocampal protein levels of these genes, cognitive functions of the rats, and histological accumulation of TAU in the brain were evaluated. Our findings in this preclinical model collectively suggest that phytochemical CuE contributes to memory gain by reducing TAU protein accumulation, which warrants further evaluation in future and studies.
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| http://dx.doi.org/10.1089/omi.2022.0175 | DOI Listing |
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