AI Article Synopsis

  • Alzheimer's disease (AD) is increasingly threatening African populations due to longer life expectancies, prompting research into natural products like catechin and dimeric procyanidins for potential cognitive protection.
  • adult male Wistar rats were used in experiments where Aβ was injected to mimic AD, followed by treatments with melatonin or the extract to assess cognitive abilities and oxidative stress levels.
  • Results showed that the extract reduced cognitive impairments and oxidative stress induced by Aβ, suggesting its potential neuroprotective effects are comparable to melatonin, but further pharmacological studies are needed to validate these findings.

Article Abstract

Objective: Alzheimer's disease (AD) is a threatening disease for African populations in the upcoming years because of the increase in their expectancy of life. Here, we investigated whether natural products from as catechin and two dimeric procyanidins (catechin + hexose) could prevent progression of oxidative stress and cognitive changes using an AD-like rat model induced by Aβ injection into the hippocampal CA1 subfield.

Methodology: Adult male Wistar rats were either microinjected with 1% ammonia as a vehicle (10 µL) or aggregated Aβ at 10 µg bilateral hippocampus. On the 14th day of post-surgery, some Aβ rats were treated with melatonin (10 mg/kg i.p.) or with the extract (300 mg/kg p.o.), and some sham-operated rats received the extract alone. Cognitive abilities were tested with Y-maze, object recognition test and Morris Water Maze. Oxidative stress markers as well as the level of activated microglial cells were assayed in the brain.

Results: Aβ rats exhibited significant deficits of recognition memory and spatial learning. This was associated with an increase of microglia Iba 1 immunoreactivity as well as nitric oxide (NO), malondialdehyde and superoxide dismutase levels but not to the thiol content in the hippocampus, prefrontal cortex and septum of AD-like rats. The extract treatment mitigated Aβ-induced cognitive impairments and reversed microglia overactivation and subsequent generation of oxidative stress markers. Interestingly, the neuroprotective actions of the extract seem to be comparable to the control drug melatonin used albeit with some more beneficial effects.

Conclusion: These findings are preliminary and should be strengthened by more pharmacological studies of bioactive compounds of before being proposed as a promising drug against AD.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8678622PMC
http://dx.doi.org/10.1515/tnsci-2020-0183DOI Listing

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