Abstract
Natural products have served humanity as a valuable source for the discovery and development of therapeutic agents. In addition, these phytochemicals can function as lead compounds for the development of synthetic analogs aimed at treating human diseases. In our aging society, Alzheimer's disease (AD) is the most common cause of dementia, which is characterized by a significant and progressive loss of memory and other cognitive functions. As society demographics change, the predominance of AD and other age-related dementias is increasing, with concurrent financial and societal costs.AD represents one of the most remarkable scientific challenges for drug discovery as the search for effective disease-modifying agents has been unsuccessful. Medicinal plants have been used for their "anti-aging" properties, and cognitive enhancing properties. In the past decades, natural products have been studied for their anti-AD properties, and their potential for developing therapeutic agents against several molecular targets has been evaluated. This insight evaluates the prospects of medicinal plants for providing disease-modifying, as well as disease-preventing, agents for AD.
Highlights
Natural products have served humanity as a valuable source for the discovery and development of therapeutic agents
The World Health Organization estimates that Alzheimer’s disease (AD) is the fourth leading cause of death affecting more than 47.5 million people worldwide, while there is a new case of dementia worldwide every 3 seconds with numbers projected to double every 20 years [1,2]
In the first formulated ‘amyloid cascade hypothesis’ of AD [12], abnormal accumulation and aggregation of the Aβ peptide derived from the amyloid precursor protein (APP) by a sequential enzymatic reaction with β- and γ-secretases lead to the formation and cerebral deposition of amyloid plaques
Summary
Its disaggregation by molecules that potentially bind on the peptide and stabilize its structure; becoming potential inhibitors of amyloidosis [27,28]. An update on AD therapeutic agents, including those targeting aggregated Aβ, aggregated tau, and neuroinflammation, is summarized in recent reviews [6, 29]. In another approach, inhibiting the formation of oligomeric fibrils and aggregates of Aβ has been examined as a therapeutic option, as recent studies suggest that the soluble, oligomeric form of Aβ is more toxic to neurons than the mature fibrils. The status of ongoing clinical studies of anti-Aβ therapies for AD and related disorders was the focus of a recent review [33] These trials include active and passive anti-Aβ immunotherapies. The latter consist of monoclonal anti-Aβ antibodies such as solanezumab and crenezumab that recognize soluble monomeric Aβ and oligomeric Aβ, respectively [33]. Patients who received aducanumab experienced significant improvements related to cognition and function, including memory, orientation, and language, leading to filing for market approval for an investigational treatment for early AD [34,35]
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