Abstract
Neurodegenerative diseases are devastating and incurable disorders characterized by neuronal dysfunction. The major focus of experimental and clinical studies are conducted on the effects of natural products and their active components on neurodegenerative diseases. This review will discuss an herbal constituent known as cinnamaldehyde (CA) with the neuroprotective potential to treat neurodegenerative disorders, such as Alzheimer's disease (AD) and Parkinson's disease (PD). Accumulating evidence supports the notion that CA displays neuroprotective effects in AD and PD animal models by modulating neuroinflammation, suppressing oxidative stress, and improving the synaptic connection. CA exerts these effects through its action on multiple signaling pathways, including TLR4/NF-κB, NLRP3, ERK1/2-MEK, NO, and Nrf2 pathways. To summarize, CA and its derivatives have been shown to improve pathological changes in AD and PD animal models, which may provide a new therapeutic option for neurodegenerative interventions. To this end, further experimental and clinical studies are required to prove the neuroprotective effects of CA and its derivatives.
Highlights
Neuroinflammation plays a critical role in the pathogenesis of both acute and chronic neurological diseases, exemplified by stroke, Alzheimer’s disease (AD), Parkinson disease (PD), and depression
The molecular mechanism of CA and its derivatives are not fully understood, but these results suggest that natural CA and its derivatives may introduce as a new candidate for further development as an anti-inflammatory agent for neurodegenerative diseases [34, 36,37,38,39,40]
It has been reported that NaB metabolized from cinnamon can inhibit the loss of Parkin and DJ-1, regulate neurotransmitter levels, and improve motor functions in mice with PD [63,64,65]
Summary
Neuroinflammation plays a critical role in the pathogenesis of both acute and chronic neurological diseases, exemplified by stroke, Alzheimer’s disease (AD), Parkinson disease (PD), and depression. Treatment or prevention of neuroinflammation-mediated neural tissue dysfunction may have a potential therapeutic option against neurological diseases [1, 2]. Herbal drugs, such as plant, spices, and their oils, have been used from ancient times to today to treat neurological disorders [3]. TCA as a main natural CA derivative significantly decreased LPS-induced neuronal death through the inhibition of neuroinflammation by blocking the nuclear factor kappa B (NF-κB) signaling pathway in vitro condition [19]. Attenuating the TLR4/NF-κB signaling pathway can be considered as a therapeutic strategy for treating brain diseases [31]. It has been revealed that CA inhibited TLR4/NF-κB
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