Almost as if by some miracle, the caffeine present in coffee can reduce drowsiness and it can increase our state of wakefulness. But the caffeine found in coffee and elsewhere (soft drinks, dark chocolate, tea etc.) is also the subject in some promising research studies. I had previously read some articles which suggested that coffee may do more than alter our state of alertness. Interestingly, it may slow the development of the Alzheimer’s Disease (AD), a form of dementia that affects about 5.4 million people in the U.S. How?
First, some background information.
One of the hallmarks of AD is the presence of extracellular plaques and intracellular neurofibrillary tangles in brain tissue. The plaques contain β-amyloid (Aβ) proteins and the tangles arise from an abnormal phosphorylation of tau protein. Eventually, the buildup of these proteins damages nerve synapses enough to cause a decline in cognition and changes in behavior. Genetic and environmental factors are both involved in the onset and level of progression of AD.
The most common form of AD (late onset) is thought to be caused by the inability to clear Aβ protein from the brain. Silverberg et al. has pointed to evidence that the production and turnover of cerebrospinal fluid (CSF) helps clear toxic molecules like Aβ from the interstitial fluid space of the brain to the blood stream. In the figure below, AD is represented by the pink rectangles and shows a lower CSF production rate than the age matched control groups PD and Acute HC.
Here is where caffeine comes in. Retrospective studies have evaluated caffeine intake in the 20 years before AD was diagnosed and it was noted that regular caffeine consumption decreased the probability that the patient would develop the disease. Caffeine may work against AD by improving the production of CSF which is known for its ability to clear away toxic molecules like Aβ proteins which cause brain tissue damage. Indeed, caffeine treatment shows higher levels of CSF production (as shown in the figure below from the article by Han and colleagues) compared to the control group. Higher levels of CSF in this study were associated with the increased expression of Na+ – K+ ATPase and increased cerebral blood flow. This Na+ – K+ ATPase is an essential driving force of CSF production by exchanging 3 Na+ ions for 2 K+ ions across the cell membrane.
You’ll see that CSF production falls with acute caffeine treatment and suggests that caffeine is effective up to a certain point. This complicates matters, since the exact mechanism for caffeine’s action via adenosine receptors to increase CSF production is not well understood. In addition, Han’s study was conducted in rats so we have to be careful with how much is extrapolated from such animal experiments. Still, these kinds of studies are something that more and more researchers are paying attention to since it is probable that caffeine is doing something to help prevent the development of AD at the neuronal level.