Abstract
The study of different natural products can provide a wealth of bioactive compounds, and more interestingly, their combination can exert a new strategy for several neurodegenerative diseases with major public health importance, such as Alzheimer’s disease (AD). Here, we investigated the synergistic neuroprotective effects of a mixed extract composed of docosahexaenoic acid, Ginkgo biloba, D-pinitol, and ursolic acid in several transgenic Caenorhabditis elegans (C. elegans) and a senescence-accelerated prone mice 8 (SAMP8) model. First, we found a significantly higher survival percentage in the C. elegans group treated with the natural product mixture compared to the single extract-treated groups. Likewise, we found a significantly increased lifespan in group of C. elegans treated with the natural product mixture compared to the other groups, suggesting synergistic effects. Remarkably, we determined a significant reduction in Aβ plaque accumulation in the group of C. elegans treated with the natural product mixture compared to the other groups, confirming synergy. Finally, we demonstrated better cognitive performance in the group treated with the natural product mixture in both AD models (neuronal Aβ C. elegans strain CL2355 and the SAMP8 mice model), confirming the molecular results and unraveling the synergist effects of this combination. Therefore, our results proved the potential of this new natural product mixture for AD therapeutic strategies.
Highlights
Alzheimer’s disease (AD) is known as a neurodegenerative disorder with major impacts among the elderly, being the most common form of dementia [1], and is estimated to affect 131 million people by 2050 [2]
This increase of reactive oxidative species (ROS) has been associated with the age-dependent reduction of antioxidant enzymes [14], resulting in altered synaptic activity and neurotransmission in neurons leading to cognitive dysfunction
We found that the natural product mixture treatment compounds, the synergistic protective effectsto of the the rest composition
Summary
Alzheimer’s disease (AD) is known as a neurodegenerative disorder with major impacts among the elderly, being the most common form of dementia [1], and is estimated to affect 131 million people by 2050 [2]. OS is caused by the overproduction of reactive oxidative species (ROS), which can damage the central nervous system (CNS) through oxygen modification of macromolecules such as lipids, proteins, and nucleic acids [13]. This increase of ROS has been associated with the age-dependent reduction of antioxidant enzymes [14], resulting in altered synaptic activity and neurotransmission in neurons leading to cognitive dysfunction. Evidence reports that the accumulation of Aβ can exacerbate mitochondrial dysfunction and ROS production, contributing to a vicious cycle [15]
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