A Preliminary Assessment of the Nutraceutical Potential of Acai Berry (Euterpe sp.) as a Potential Natural Treatment for Alzheimer's Disease

Abstract

Alzheimer's disease (AD) is characterised by progressive neuronal atrophy and the loss of neuronal function as a consequence of multiple pathomechanisms. Current AD treatments primarily operate at a symptomatic level to treat a cholinergic deficiency and can cause side effects. Hence, there is an unmet need for healthier lifestyles to reduce the likelihood of AD as well as improved treatments with fewer adverse reactions. Diets rich in phytochemicals may reduce neurodegenerative risk and limit disease progression. The native South American palm acai berry (Euterpe oleraceae) is a potential source of dietary phytochemicals beneficial to health. This study aimed to screen the nutraceutical potential of the acai berry, in the form of aqueous and ethanolic extracts, for the ability to inhibit acetyl- and butyryl-cholinesterase (ChE) enzymes and scavenge free radicals via 2,2-diphenyl-1-picryl-hydrazyl-hydrate (DPPH) or 2,2'-azino-bis-3-ethylbenzthiazoline-6-sulphonic acid (ABTS) assays. In addition, this study aimed to quantify the acai berry's antioxidant potential via hydrogen peroxide or hydroxyl scavenging, nitric oxide scavenging, lipid peroxidation inhibition, and the ability to reduce ferric ions. Total polyphenol and flavonoid contents were also determined. Acai aqueous extract displayed a concentration-dependent inhibition of acetyl- and butyryl-cholinesterase enzymes. Both acai extracts displayed useful concentration-dependent free radical scavenging and antioxidant abilities, with the acai ethanolic extract being the most potent antioxidant and displaying the highest phenolic and flavonoid contents. In summary, extracts of the acai berry contain nutraceutical components with anti-cholinesterase and antioxidant capabilities and may therefore provide a beneficial dietary component that limits the pathological deficits evidenced in AD.

Keywords: Alzheimer’s disease; Euterpe oleraceae; acai berry; antioxidant; cholinesterase inhibitors; nutraceuticals.

Figure 1

Cholinesterase inhibition by acai aqueous and ethanolic extracts. AChE inhibitory activity of acai aqueous extract (A) and acai ethanolic extract (B). BuChE inhibitory activity of acai aqueous extract (C) and acai ethanolic extract (D). Histograms represent means ± SEM for at least three replicate assays at each extract concentration (n = 6). For the positive control inhibitors, 5 mM azamethiphos and 5 mM ethopropazine hydrochloride were used for AChE and BuChE, respectively. For marked significance * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

Figure 2

DPPH radical scavenging activity of acai aqueous and ethanolic extracts. Acai antioxidant activity was assessed via the percentage inhibition (radical scavenging) of DPPH over a concentration range of 0.01–4000 µg/mL (A) and 0.01–10 µg/mL (B). Assays were performed in triplicate at each extract concentration (n = 6).

Figure 3

ABTS^•+ scavenging activity of acai aqueous and ethanolic extracts. Acai antioxidant activity was assessed as a percentage inhibition (radical scavenging) of ABTS over a concentration range of 1–1000 µg/mL. Assays were performed in triplicate at each extract concentration (n = 6).

Figure 4

H₂O₂ scavenging activity of acai aqueous and ethanolic extracts. Acai antioxidant activity was assessed as a percentage of the scavenging activity of H₂O₂ over a concentration range of 1–4000 µg/mL. Assays were performed in triplicate at each extract concentration (n = 6).

Figure 5

Hydroxyl radical scavenging activity of acai aqueous and ethanolic extracts. Acai antioxidant activity was assessed via the percentage of the scavenging of ^•OH. Assays were performed in triplicate at each extract concentration (n = 6).

Figure 6

Nitric oxide (^•NO) scavenging activity of acai aqueous and ethanolic extracts. Acai antioxidant activity was assessed via the percentage of the scavenging of ^•NO. Assays were performed in triplicate at each extract concentration (n = 6).

Figure 7

Lipid peroxidation inhibitory activity of acai aqueous and ethanolic extracts. Acai antioxidant activity was assessed via the percentage of the inhibition of malondialdehyde (MDA) production. Assays were performed in triplicate at each extract concentration (n = 6).

Figure 8

Reductive capacity of different concentrations of plant extracts from acai berry. Plant reducing power was measured by the ability to reduce ferric (Fe³⁺) to ferrous (Fe²⁺) iron (OD density change at 700 nm). The positive control was L-ascorbic acid (vitamin C). Assays were performed in triplicate at each extract concentration (n = 6).