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. 2022;20(8):1498-1518.
doi: 10.2174/1570159X20666211217163540.

Natural Product-based Nanomedicine: Recent Advances and Issues for the Treatment of Alzheimer's Disease

Choy Ker Woon  1 , Wong Kah Hui  2 , Razif Abas  3 , Muhammad Huzaimi Haron  4 , Srijit Das  5 , Teoh Seong Lin  6
Affiliations

Natural Product-based Nanomedicine: Recent Advances and Issues for the Treatment of Alzheimer's Disease

Choy Ker Woon et al. Curr Neuropharmacol. 2022.

Abstract

Alzheimer's disease (AD) affects the elderly and is characterized by progressive neurodegeneration caused by different pathologies. The most significant challenges in treating AD include the inability of medications to reach the brain because of its poor solubility, low bioavailability, and the presence of the blood-brain barrier (BBB). Additionally, current evidence suggests the disruption of BBB plays an important role in the pathogenesis of AD. One of the critical challenges in treating AD is the ineffective treatments and their severe adverse effects. Nanotechnology offers an alternative approach to facilitate the treatment of AD by overcoming the challenges in drug transport across the BBB. Various nanoparticles (NP) loaded with natural products were reported to aid in drug delivery for the treatment of AD. The nano-sized entities of NP are great platforms for incorporating active materials from natural products into formulations that can be delivered effectively to the intended action site without compromising the material's bioactivity. The review highlights the applications of medicinal plants, their derived components, and various nanomedicinebased approaches for the treatment of AD. The combination of medicinal plants and nanotechnology may lead to new theragnostic solutions for the treatment of AD in the future.

Keywords: Alzheimer’s disease; amyloid-β; blood-brain barrier; drug delivery; nanoparticles; phytochemicals.

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Figures

Fig. (1)
Fig. (1)
The disruption of the BBB and dysregulated transport networks contribute to the development of neurodegenerative alterations, the accumulation of Aβ and tau pathology, and neuronal death, as shown in this graphical abstract of AD animal model. Breakdown of the BBB causes perivascular buildup of blood-derived neurotoxic chemicals which lead to oxidant stress in neurons (1) and eventually contributing to hypoperfusion, edema and tissue hypoxia (2). BBB disintegration is caused by degradation of BBB tight connection and basement membrane molecules (3). A loss of equilibrium between Aβ efflux and influx over the BBB occurs when BBB transport is disrupted (4). The downregulation of BBB GLUT1 transporter hastens the breakdown of the BBB and the development of Aβ pathology, as well as tau pathology and neuronal death (5). The elevated RAGE expression at the BBB also contributes to Aβ buildup in the brain (6).
Fig. (2)
Fig. (2)
Phytochemical for the natural product involved in AD.
See this image and copyright information in PMC

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