Abstract

BackgroundAlzheimer's disease (AD) is a multifactorial neurological disease with neurofibrillary tangles and neuritic plaques as histopathological markers. Due to this, although AD is the leading cause of dementia worldwide, clinical AD dementia cannot be certainly diagnosed until neuropathological post-mortem evaluation. Coffee has been reported to have neurologically protective factors, particularly against AD, but coffee brand and type have not been taken into consideration in previous studies. We examined the discrepancies among popular commercial and instant coffees in limiting the development and progression through Aβ1-40 and Aβ1-42 production, and hypothesized that coffee consumption, regardless of brand or type, is beneficial for stalling the progression and development of Aβ-related AD.MethodsCoffee samples from four commercial coffee brands and four instant coffees were purchased or prepared following given instructions and filtered for the study. 5, 2.5, and 1.25% concentrations of each coffee were used to treat N2a/APPswe cell lines. MTT assay was used to assess cell viability for coffee concentrations, as well as pure caffeine concentrations. Sandwich ELISA assay was used to determine Aβ concentration for Aβ1-40 and Aβ1-42 peptides of coffee-treated cells.ResultsCaffeine concentrations were significantly varied among all coffees (DC vs. MDC, PC, SB, NIN, MIN p < 0.05). There was no correlation between caffeine concentration and cell toxicity among brands and types of coffee, with no toxicity at 0.5 mg/ml caffeine and lower. Most coffees were toxic to N2a/APPswe cells at 5% (p < 0.05), but not at 2.5%. Most coffees at a 2.5% concentration reduced Aβ1-40 and Aβ1-42 production, with comparable results between commercial and instant coffees.ConclusionAll coffees tested have beneficial health effects for AD through lowering Aβ1-40 and Aβ1-42 production, with Dunkin' Donuts® medium roast coffee demonstrating the most consistent and optimal cell survival rates and Aβ concentration. On the other hand, Starbucks® coffee exhibited the highest cell toxicity rates among the tested coffees.

Highlights

  • Alzheimer’s Disease (AD) is a neurodegenerative disease that is marked by the gradual deterioration of memory and cognition, among other cognitive impairments, which are attributed to extracellular aggregates of Aβ plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau protein [1, 2]

  • PC and SBC had significantly greater caffeine concentrations compared to DC and MDC, and FIN and SBIN had significantly greater caffeine concentrations compared to MIN and NIN (DC vs. MDC, PC, SB p < 0.05; FIN vs. MIN, NIN p < 0.05; MIN vs. SBIN p < 0.05)

  • Little is known about the potential differences in coffee brand and brew type, health consequences relating to AD

Read more

Summary

Introduction

Alzheimer’s Disease (AD) is a neurodegenerative disease that is marked by the gradual deterioration of memory and cognition, among other cognitive impairments, which are attributed to extracellular aggregates of Aβ plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau protein [1, 2]. AD is the most common form of dementia and is the sixth leading cause of death in the United States [3]. 6 million Americans are currently living with AD, and this number is expected to rise to nearly 13 million by 2050 [3, 5, 6]. These statistics are mirrored by an increasing economic burden; the Alzheimer’s Association estimates that in 2018, AD and other forms of dementia will cost the United States $277 billion [7]. An estimated 16.1 million Americans provide unpaid assistance for patients with AD and other forms of dementia [3] This unpaid care primarily comes from loved ones of patients, who are financially and emotionally burdened by the disease. We examined the discrepancies among popular commercial and instant coffees in limiting the development and progression through Aβ1-40 and Aβ1-42 production, and hypothesized that coffee consumption, regardless of brand or type, is beneficial for stalling the progression and development of Aβ-related AD

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call