Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder affecting more than 35 million people worldwide. As the prevalence of AD is dramatically rising, there is an earnest need for the identification of effective therapies. Available drug treatments only target the symptoms and do not halt the progression of this disorder; thus, the use of natural compounds has been proposed as an alternative intervention strategy. Icariin, a prenylated flavonoid, has several therapeutic effects, including osteoporosis prevention, sexual dysfunction amelioration, immune system modulation, and improvement of cardiovascular function. Substantial studies indicate that icariin may be beneficial to AD by reducing the production of extracellular amyloid plaques and intracellular neurofibrillary tangles and inhibiting phosphodiesterase-5 activity. Moreover, increasing evidence has indicated that icariin exerts a protective role in AD also by limiting inflammation, oxidative stress and reducing potential risk factors for AD such as atherosclerosis. This mini-review discusses the multiple potential mechanisms of action of icariin on the pathobiology of AD including explanation regarding its bioavailability, metabolism and pharmacokinetic.
Highlights
Alzheimer’s disease (AD) is a progressive irreversible neurodegenerative disease that is becoming a population aging-related concern for public health systems all over the world due to its direct and indirect costs (Dos Santos et al, 2018)
BACE1 cleaves amyloid precursor proteins (APP), producing an APP C-terminal fragment, which is subsequently cleaved within the transmembrane domain by γ-secretase at 40 or 42 residues, leading to the release of two different amyloid β peptide (Aβ) peptides Aβ1−40 or the most abundant Aβ1−42 (Thal et al, 2015) due to the variability in the C-terminus of Aβ (Tamagno et al, 2005)
Beside Aβ plaques and neurofibrillary tangles (NFTs), more than 50% of AD patients exhibit concurrent α-synuclein pathology (Twohig et al, 2018). α-synuclein is a 140 amino-acid protein abundantly expressed in neuronal presynaptic terminals
Summary
Alzheimer’s disease (AD) is a progressive irreversible neurodegenerative disease that is becoming a population aging-related concern for public health systems all over the world due to its direct and indirect costs (Dos Santos et al, 2018). It has been shown that brain tissues in AD patients are exposed to oxidative stress (Gella and Durany, 2009), a condition characterized by an imbalance between ROS production and the endogenous antioxidative defense system Another very common feature of patients with AD is vascular dysfunction (Iadecola, 2005). Phosphodiesterase-5 inhibitors might interfere with the pathophysiological processes of AD such as neurovascular dysfunction (Sabayan et al, 2010) They can exert their positive effect on learning and memory by activating the NO/cGMP pathway (Puzzo et al, 2009) that produces a regulatory effect on endothelial function by relaxing blood vessels (Schulz et al, 2002). Substantial studies indicate that icariin and its metabolites may be beneficial to AD by reducing the production of extracellular amyloid plaques and intracellular NFTs and inhibiting phosphodiesterase-5 activity. Icariin has been found to possess multiple neuroprotective effects: it improves survival and function of neurons (Guo et al, 2010; Li F. et al, 2010) and triggers their self-renewal through neural stem cells (Huang et al, 2014)
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