Beyond catchiness, some very interesting research reveals that moderate consumption of coffee can help to clear beta amyloid from the brain. (“Beta amyloid denotes peptides of 36–43 amino acids that are crucially involved in Alzheimer’s disease as the main component of the amyloid plaques found in the brains of Alzheimer patients.”)
Building the case that coffee consumption prevents Alzheimer’s, it is noted in “Caffeine Suppresses Amyloid-B Levels in Plasma and Brain of Alzheimer’s Disease Transgenic Mice” that:
Recent longitudinal studies spanning 4–10 years suggest that habitual caffeine/coffee intake protects against cognitive impairment in aging humans. Moreover, an epidemiological study evaluated caffeine intake during the 20 years preceding AD (Alzheimer’s disease) diagnosis and found that AD patients consumed markedly less caffeine during that period compared to age-matched individuals without AD. Collectively, these and other observational human studies suggest that habitual caffeine/coffee intake may protect against memory impairment and AD during aging.
Epidemiological studies are valuable and telling, but they are not controlled and drawing causal conclusions from them is difficult. The next step in the research process would be to see how animals react. In mouse studies, it has been found that regular administration of caffeine to mice that had a genetic predisposition toward Alzheimer’s development (APPsw mice), showed that caffeine prevented Alzheimer’s disease development. Specifically, the researchers found that caffeine “1) protected these mice from otherwise certain cognitive impairment in older age, and 2) limited their brain production of the peptide β-amyloid (Aβ). The moderate amount of caffeine intake given to these APPsw mice (human equivalency of 5 cups of coffee per day) suppressed both β-secretase (BACE1) and γ-secretase/PS1 levels in hippocampus, indicating that caffeine can directly impact AD pathogenesis in these AD mice.”
In another study, “Beneficial effects of caffeine in a transgenic model of Alzheimer’s disease-like tau pathology” published in Neurobiology and Aging in 2014, it was noted that regular caffeine consumption broke up tau deposits, along with beta-amyloid plaques, two of the dominant characteristics of Alzheimer’s affected brains.
Of course, we’re not mice and five cups of coffee seems a bit excessive, but the combination of the epidemiological data and rodent data suggest there might be something to the caffeine – Alzheimer’s connection. Add that to the correlational data with humans showing that people who drink coffee regularly are less likely to develop Alzheimer’s disease and we have strong case for regular consumption of caffeine (especially coffee – other sources of caffeine have been less strongly linked to Alzheimer’s prevention) throughout adulthood in order to prevent Alzheimer’s in later life. The next step is clinical trials in humans and those have been initiated. Until those results are in, we can only postulate a connection.
It should be noted that the anti-Alzheimer’s disease drugs that are currently on the market, cholinesterase inhibitors and NMDA receptor antagonists, show far less efficacy at treating or preventing Alzheimer’s disease than caffeine/coffee. Both cholinesterase inhibitor and NMDA receptor antagonist drugs “have minimal benefits and do not appear to address AD pathogenesis.” Neither cholinesterase inhibitor nor NMDA receptor antagonist drugs reduce tau deposits or beta-amyloid plaques. Caffeine does. Given that caffeine is safe for most people, readily available, inexpensive and has minimal side-effects and that cholinesterase inhibitor and NMDA receptor antagonist drugs have none of those benefits – regular coffee consumption may be an interesting option for treating and preventing Alzheimer’s.
Good job, big pharma. That’s why you’re paid the big bucks – to create drugs that are less effective (and far more dangerous) than a $1 cup of McDonalds coffee.
- Journal of Alzheimer’s Disease, “Caffeine suppresses β-amyloid levels in plasma and brain of Alzheimer’s transgenic mice”
- Journal of Alzheimer’s Disease, “Caffeine reverses cognitive impairment and decreases brain amyloid-beta levels in aged Alzheimer’s disease mice.”
- Neurobiology of Aging, “Beneficial effects of caffeine in a transgenic model of Alzheimer’s disease-like tau pathology”
- Journal of Alzheimer’s Disease, “Caffeine as a protective factor in dementia and Alzheimer’s disease.”
- Journal of Alzheimer’s Disease, “Caffeine and Coffee as Therapeutics Against Alzheimer’s Disease”
- Science Daily, “Caffeine against Alzheimer’s disease? Positive effect on tau deposits demonstrated”
About the Author: Lisa Bloomquist was “Floxed” on her 32nd birthday by Cipro, a fluoroquinolone antibiotic. After 2 years of battling the mysterious health ailments that come with an adverse reaction to a fluoroquinolone, she has fought her way back to health. She is now fighting for recognition of the harm that these drugs can cause and hoping to help those who are suffering from them through their fluoroquinolone induced illness to find recovery. Her web site, Floxie Hope, highlights stories of hope and recovery. Mito Madness, also started by Lisa, focuses on the absurdity of ignoring the role of mitochondria in forming disease models.