Coffee And Health: Cognitive Health. Caffeine’s acute effects were discussed in the section on mental performance. This section will examine the long-term impact of caffeine on the prevention of cognitive degenerative diseases. Cognitive talents such as linguistic ability, inductive reasoning, and perceptual quickness diminish around age 20.
Genetics, life experiences, and lifestyle variables all impact the rate and extent of this decrease (Hedden and Gabrieli, 2004). Arab et al., 2013; Ritchie et al., 2007; Corley et al., 2010) describe a large body of epidemiological data that establishes a relationship between regular coffee consumption and a decreased risk of cognitive decline in the elderly.
A meta-analysis of these human studies demonstrates that caffeine, not coffee, has a specific protective effect (Santos et al., 2010; Ryan et al., 2002).
However, animal models of neurological disease and aging are beginning to demonstrate a link between chlorogenic acids and their prevention (Esposito et al., 2002; Ramassamy, 2006).
Alzheimer’s disease is the most frequent cause of dementia, since it results in gradual cognitive decline. Although there is no cure for Alzheimer’s disease at the moment (Waite, 2015), research have discovered a relationship between coffee consumption and the development of the illness, with a 27% risk decrease (Waite, 2015).
Caffeine’s anti-inflammatory actions on the A1 and A2 receptors, as well as the decrease of damaging beta-amyloid peptide deposits in the brain, which is a pathogenic characteristic of Alzheimer’s disease patients, are likely to be involved in the process (Rosso et al., 2008; Arendash and Cao, 2010).
Along with coffee, polyphenols seem to have an anti-disease impact on Alzheimer’s disease. While the effect of coffee polyphenols on human cognitive function has not been completely researched, the number of findings about polyphenols’ in vitro neuroprotective capabilities is rapidly growing (Lakey-Beitia et al., 2015).
Although the mechanisms are unclear, anti-inflammatory activities of polyphenols seem to have a role in the prevention of Alzheimer’s disease. Additional hypotheses include (1) blocking acetylcholinesterase and butyrylcholinesterase in the brain, which slows the breakdown of acetylcholine and butyrylcholine, and (2) reducing oxidative stress-induced neurodegeneration owing to its significant antioxidative activity (Oboh et al., 2013).
Numerous epidemiological studies have shown an inverse relationship between caffeine use and the risk of developing Parkinson’s disease related to Alzheimer’s disease. The latter is a neuropathological condition that results in resting tremors and impaired motor performance.
Symptoms include muscle stiffness, irregular walking, and poor postural reflexes. Neuronal degeneration in the brainstem is implicated (Kuwana et al., 1999).
Coffee consumption seems to have a beneficial effect on the course of Parkinson’s disease. According to a meta-analysis of 26 studies, coffee users had a 25% reduced incidence of Parkinson’s disease than non-coffee drinkers. Caffeine’s capacity to suppress the brain’s A2 adenosine receptors is almost certainly the mechanism (Costa et al., 2010).
Another possible additional mechanism was recently discovered during the investigation. Trigonelline appears to have neuroprotective properties in a mouse model, reversing significant motor impairment (Nathan et al., 2014).