Abstract
Neurodegenerative diseases (NDs) are one of major public health problems and their impact is continuously growing. Curcumin has been proposed for the treatment of several of these pathologies, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) due to the ability of this molecule to reduce inflammation and aggregation of involved proteins. Nevertheless, the poor metabolic stability and bioavailability of curcumin reduce the possibilities of its practical use. For these reasons, many curcumin derivatives were synthetized in order to overcome some limitations. In this review will be highlighted recent results on modification of curcumin scaffold in the search of new effective therapeutic agents against NDs, with particular emphasis on AD.
Highlights
For last two centuries, natural occurring products have attracted the attention of many researchers due to their health benefits in the prevention and treatment of several diseases [1]
A common characteristic of age-related neurodegenerative diseases, including Alzheimer’s disease (AD), is the pathological accumulation of unfolded and aggregation-prone proteins in the brain, which are considered the major cause of synaptic loss and progressive neuronal death observed in these disorders [18]
Increasing evidence suggests that synaptic dysfunction and neuronal loss precede the formation of neurofibrillary tangles (NFTs) [34,35,36,37,38,39], indicating that the smaller and prefibrillar aggregates, tau oligomers, may be responsible for the toxic effects during the early stage of AD and other tauopathies [40,41]
Summary
Natural occurring products have attracted the attention of many researchers due to their health benefits in the prevention and treatment of several diseases [1]. A common characteristic of age-related neurodegenerative diseases, including AD, is the pathological accumulation of unfolded and aggregation-prone proteins in the brain, which are considered the major cause of synaptic loss and progressive neuronal death observed in these disorders [18]. Increasing evidence suggests that synaptic dysfunction and neuronal loss precede the formation of NFTs [34,35,36,37,38,39], indicating that the smaller and prefibrillar aggregates, tau oligomers, may be responsible for the toxic effects during the early stage of AD and other tauopathies [40,41]. Curcumin has been shown to attenuate amyloid-β aggregate-associated neurotoxicity by promoting the formation of “off-pathway” nontoxic soluble oligomers and prefibrillar proteins [47]. This review attempts to explore the protective role of curcumin and its related compounds in the treatment of neurodegenerative disorders as a potential modulator of pathogenic pathways associated with AD and related diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
