Abstract
Patients suffering from Alzheimer’s disease (AD) are still increasing worldwide. The development of (AD) is related to oxidative stress and genetic factors. This study investigated the therapeutic effects of ellagic acid (EA) on the entorhinal cortex (ERC), which plays a major role in episodic memory, in the brains of an AD rat model. AD was induced using AlCl3 (50 mg/kg orally for 4 weeks). Rats were divided into four groups: control, AD model, EA (treated with 50 mg/kg EA orally for 4 weeks), and ADEA (AD rats treated with EA after AlCl3 was stopped) groups. All rats were investigated for episodic memory using the novel object recognition test (NORT), antioxidant serum biomarkers, lipid peroxidation, histopathology of the ERC, and quantitative PCR for the superoxide dismutase (SOD) gene. EA therapy in AD rats significantly increased the discrimination index for NORT and the levels of SOD, glutathione, and total antioxidant capacity. Lipid peroxidation products were decreased, and the neurofibrillary tangles and neuritic plaques in the ERC sections were reduced after EA administration. The decrease in ERC thickness in the AD group, caused by caspase-3-mediated apoptosis and neurotoxicity due to amyloid precursor protein, was modulated by the increased SOD mRNA expression. Adjustment of the ERC antioxidant environment and decreased oxidative stress under EA administration enhanced SOD expression, resulting in the modulation of amyloid precursor protein toxicity and caspase-3-mediated apoptosis, thereby restoring episodic memory.
Highlights
Dementia causes a continuous decline in cognitive function and is associated with an increased burden on patients’ families and on society [1]
ADEA rats explored N for a mean of 14.4 ± 0.84 s, which was an increase from 7.3 ± 0.48 s in Alzheimer’s disease (AD) rats
The discrimination index (DI) increased significantly in the ADEA group compared to the AD group (p ≤ 0.05) (Figure 1a–c)
Summary
Dementia causes a continuous decline in cognitive function and is associated with an increased burden on patients’ families and on society [1]. Alzheimer’s disease (AD), a common cause of dementia [2], is a neurodegenerative disorder that leads to impaired memory, a decline in mental functions, behavioral problems, and neuropsychiatric manifestations [3]. AD is correlated with the autosomal dominant or sporadic inheritance of genes associated with amyloid precursor protein (APP), apolipoprotein E, and presenilin 1 and 2 [5]. An increase in APP levels has been associated with AD neurodegenerative changes and plaque formation in the brain. Excessive precipitation of amyloid plaques and microglia activity are associated with deterioration of cognition [6]
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