Neuroprotective and Neurodegenerative Aspects of Coffee and Its Active Ingredients in View of Scientific Literature.

Shehnaz Wasim,Vanessa M Awad,Sirisha Sakhamuru,Bilal Haider Malik,Vishal Kukkar

doi:10.7759/cureus.9578

Abstract

Coffee and its components have several neuroprotective properties that lower the risk of cognitive decline and other neurodegenerative diseases. This study reviews the mechanisms by which coffee and its respective compounds affect the brain and its pathologies. Many epidemiological studies in this literature review have shown coffee to reduce the risk of developing dementia, stroke, and Alzheimer's disease. It may also have a positive impact on the disease course of amyotrophic lateral sclerosis, Parkinson's disease, and depression. The optimal benefits achieved from coffee in these pathologies rely on higher daily doses. Most of its effects are attributed to caffeine by the antagonism of adenosine receptors in the central nervous system; however, other coffee constituents like chlorogenic acids have also shown much promise in therapeutic value. Existing research considers coffee to have great potential, but additional studies are still needed to clarify the mechanisms and actual causal relationships in certain neuropathologies.

Highlights

BackgroundCoffee is one of the most popular beverages
Many epidemiological studies in this literature review have shown coffee to reduce the risk of developing dementia, stroke, and Alzheimer's disease
Most of its effects are attributed to caffeine by the antagonism of adenosine receptors in the central nervous system; other coffee constituents like chlorogenic acids have shown much promise in therapeutic value

Summary

Introduction

Coffee is one of the most popular beverages. On average, Americans drink about two cups of coffee everyday [1]. Several studies have suggested that coffee is associated with reduced risks of developing AD [16] This could be due to the effects of caffeine and CGAs on the adenosine receptors that play a role in preventing toxic β-amyloid peptide deposits in the brain [37]. The local antioxidant property of CGAs aids in neurogenesis and together with pyrogallol, trigonelline, catechol, 5-hydroxytryptamides, and N-methylpyridinium exhibits similar effects by increasing calcium signaling and dopamine release in the central nervous system [13,41] Another explanation is that coffee raises the number of bifidobacteria that are associated with mitigating local inflammatory response, diminishing procarcinogenic processes and lower misfolding rates of α-synuclein in the enteric nervous system, reducing the risk of PD by decreasing dissemination of the protein to the brain [45]. The correlation in these patients was with higher cerebral spinal fluid caffeine levels [46]

Conclusions

Disclosures

13. Nehlig A

Findings

48. Larsson SC