Abstract
Aim: The current study hypothesizes that ingestion of polyphenols-enriched preparation such as yeast fermented extracts of green and roasted coffee beans will demonstrate neuroprotective and stimulatory function.
 Study Design: Optimizing yeast (Saccharomyces cerevisiae) mediated fermentation conditions of C.Arabica beans →Extraction by the sonication-agitation method before and after roasting to obtain Fermented Green Coffee Extracts (FGCE) and Fermented Roasted Coffee Extracts (FRCE) →Phytochemical profiling of the fermented extracts was performed → Animal Study (in vivo evaluation).
 Place and Duration: The research work was conducted during December, 2019 to May, 2020 at the Department of Biotechnology, Sri Venkateswara College of Engineering, Post Bag No.1, Pennalur, Sriperumbudur Tk, Kancheepuram Dt TN-602117, India.
 Methodology: The FGCE and FRCE extracts were prepared and subjected to comparative phytochemical profiling for in vitro analysis. Further, the in vivo analysis was performed on 24 Albino Wistar rats, which were divided into four groups (Group I (Control group) received normal diet; Group II (AD induced group) received AlCl3; Group III received FGCE and AlCl3, Group IV received FRCE and AlCl3). In order to represent the most exact model that mimics AD the rats were injected with AlCl3 .6H2O at dose 70 mg / kg I.P for 6 weeks. During induction the rats were subjected to spatial memory tests (T-maze) and motor co-ordination tests (burrowing assay).
 Results: The FGCE had a higher amount of polyphenols (1.20 ± 0.02 GAE mg / ml) compared to FRCE (0.99 ± 0.047 GAE mg / ml). Also, the ferric reducing anti-oxidant potential was higher in FGCE (5.14 ± 0.17 mmol Fe2+ / g) than in FRCE (3.7 ± 0.2 mmol Fe2+ / g). As a result of behavioural analysis, the fermented green coffee extract consumption in Alzheimer induced rats had a prominent positive effect on memory retention and motor co-ordination.
 Conclusion: This study elucidates the potential nature of FGCE in decelerating the progression of AD at a higher rate than FRCE.
Highlights
Considering the impact of the various sociodemographic transitions in the world, especially the fortuitous increase in lifespan over the last decades has lead to an increase in the risk of age-related cognitive impairments such as dementia, including neurodegenerative diseases, e.g. Alzheimer’s disease (AD) and Parkinson’s disease (PD)
There were significant differences between the Total polyphenol content (TPC) of all four extracts (GCE, roasted coffee extracts (RCE), Fermented Green Coffee Extracts (FGCE), Fermented Roasted Coffee Extracts (FRCE) represented by a, b, c, d respectively) due to factors like roasting and fermentation
The phenolic contend tends to increase in the fermented coffee extracts [29,30]. (ii)With an increase in roasting temperature, degradation of phenolic content occurs and gets associated with melanoidins; the contribution of Chlorogenic Acid (CGA) to the antioxidant activity of the whole green coffee extract was higher than that of melanoidin-bound phenolic compounds in roasted extracts [31]
Summary
Considering the impact of the various sociodemographic transitions in the world, especially the fortuitous increase in lifespan over the last decades has lead to an increase in the risk of age-related cognitive impairments such as dementia, including neurodegenerative diseases, e.g. Alzheimer’s disease (AD) and Parkinson’s disease (PD). The pathophysiology of AD encompasses the accumulation of Amyloid-beta plaques (Aβ) which are extracellular deposits of Aβ in the brain parenchyma and in the cerebral blood vessels where it is known as cerebral amyloid angiopathy (CAA) Another possibility is the presence of neurofibrillary tangles (NFT) composed largely of paired helical tangles that disturb the cytoskeleton by disrupting cell structure destroying axonal transport and synaptic viability leading to neuronal dysfunction [2]. The main focus of AD treatment by novel pharmacotherapies is to deplete Aβ production through the inhibition of β and γ secretase enzymes; and to induce dissolution of existing cerebral Aβ plaques. These approaches attempting to treat these lesions have not achieved permanent successful results. Investigating strategies that may prevent or delay the progression of Alzheimer’s disease is a matter of the utmost importance [3]
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