Abstract
Alzheimer’s disease (AD) is the most common form of dementia, characterized by chronic neuron loss and cognitive problems. Aggregated amyloid beta (Aβ) peptides, a product of cleaved amyloid precursor protein (APP) by beta-secretase 1 (BACE-1), have been indicated for the progressive pathogenesis of AD. Currently, screening for anti-AD compounds in foodstuffs is increasing, with promising results. Hence, the purpose of this study was to investigate the extraction conditions, phytochemical contents, and anti-AD properties, targeting Aβ peptides of Morus cf. nigra ‘Chiang Mai’ (MNCM) both in vitro and in vivo. Data showed that the aqueous extract of MNCM contained high amounts of cyanidin, keracyanin, and kuromanin as anthocyanidin and anthocyanins. The extract also strongly inhibited cholinesterases and BACE-1 in vitro. Moreover, MNCM extract prevented Aβ-induced neurotoxicity and promoted neurite outgrowth in neuronal cells. Interestingly, MNCM extract reduced Aβ1–42 peptides and improved locomotory coordination of Drosophila co-expressing human APP and BACE-1, specifically in the brain. These findings suggest that MNCM may be useful as an AD preventive agent by targeting Aβ formation.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia and a public health concern worldwide
Loss of cholinergic neurons located in the basal forebrain leads to reduced production of the neurotransmitter, acetylcholine, which is involved in memory and cognitive functions
To optimize the extraction conditions regarding anti-AD properties of Morus cf. nigra ‘Chiang Mai’ (MNCM), aqueous ethanol was utilized as a solvent for anthocyanins extraction
Summary
Alzheimer’s disease (AD) is the most common form of dementia and a public health concern worldwide. AD is the fifth leading cause of death among people over 65 years old [1] and growth of AD prevalence is expected. In the USA, the care cost for dementia patients has been estimated at $290 billion, rendering a huge economic problem for society [2]. AD is a chronic neurodegenerative disorder that is characterized by the loss of cholinergic neurons, low levels of acetylcholine, and aggregation of neurotoxic amyloid beta plaque. Loss of cholinergic neurons located in the basal forebrain leads to reduced production of the neurotransmitter, acetylcholine, which is involved in memory and cognitive functions. Inhibition of acetylcholine-degrading enzymes, cholinesterases (acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)), may improve attention span and cognitive ability [3]
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