The Missing Link between Coffee and Neuroprotection: Is it the Caffeine or Another Component?
BACKGROUND AND PURPOSE:
Coffee is associated with decreased risk of Alzheimer’s disease (AD) and Parkinson’s disease (PD)
Mancini et al. (Frontiers in Neuroscience, 2018) sought to determine whether compounds found in brewed coffee may elicit neuroprotective effects by inhibiting the aggregation of amyloid-beta (Aβ) and tau (AD) or α-synuclein (PD)
The study tested the impact of
3 instant coffee extracts
Light roast | Dark roast | Decaffeinated dark roast
6 coffee components
Investigators measured components ability to inhibit the fibrillization of Aβ and tau proteins
Instant coffee extracts (all roast levels)
Inhibit fibrillization of Aβ and tau
Promote α-synuclein oligomerization
Dark roast coffee extracts are more potent inhibitors of Aβ oligomerization
Pure caffeine has no effect on Aβ, tau or α-synuclein aggregation
Chlorogenic acid, Caffeic acid and Quercetin inhibit the fibrillization of Aβ
Only Quercetin inhibits Aβ oligomerization
Phenylindane is a potent inhibitor of both Aβ and tau fibrillization, and also inhibits Aβ oligomerization
Caffeic acid and Quercetin promote the aggregation of α-synuclein at concentrations
No other coffee components affect α-synuclein oligomerization
Coffee components may be neuroprotective through their interaction with Aβ and tau aggregation
Phenylindane was identified as a dual-inhibitor of both pathogenic Aβ and tau aggregation
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