"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
- Caffeine -

General Information:

Wikipedia entry: 



Caffeine May Slow Alzheimer's Disease and Other Dementias, Restore Cognitive Function, According to New Evidence

ScienceDaily (May 17, 2010) Although caffeine is the most widely consumed psychoactive drug worldwide, its potential beneficial effect for maintenance of proper brain functioning has only recently begun to be adequately appreciated. Substantial evidence from epidemiological studies and fundamental research in animal models suggests that caffeine may be protective against the cognitive decline seen in dementia and Alzheimer's disease (AD)...


Caffeine protects Alzheimer's mice against cognitive impairment and reduces brain beta-amyloid production.
Arendash GW, Schleif W, Rezai-Zadeh K, Jackson EK, Zacharia LC, Cracchiolo JR,
Shippy D, Tan J.
The Byrd Alzheimer's Center and Research Institute, Tampa, FL 33647, USA.
Neuroscience. 2006 Nov 3;142(4):941-52. Epub 2006 Aug 28.

A recent epidemiological study suggested that higher caffeine intake over decades reduces the risk of Alzheimer's disease (AD). The present study sought to determine any long-term protective effects of dietary caffeine intake in a controlled longitudinal study involving AD transgenic mice. Caffeine (an adenosine receptor antagonist) was added to the drinking water of amyloid precursor protein, Swedish mutation (APPsw) transgenic (Tg) mice between 4 and 9 months of age, with behavioral testing done during the final 6 weeks of treatment. The average daily intake of caffeine per mouse (1.5 mg) was the human equivalent of 500 mg caffeine, the amount typically found in five cups of coffee per day. Across multiple cognitive tasks of spatial learning/reference memory, working memory, and recognition/identification, Tg mice given caffeine performed significantly better than Tg control mice and similar to non-transgenic controls. In both behaviorally-tested and aged Tg mice, long-term caffeine administration resulted in lower hippocampal beta-amyloid (Abeta) levels. Expression of both Presenilin 1 (PS1) and beta-secretase (BACE) was reduced in caffeine-treated Tg mice, indicating decreased Abeta production as a likely mechanism of caffeine's cognitive protection. The ability of caffeine to reduce Abeta production was confirmed in SweAPP N2a neuronal cultures, wherein concentration-dependent decreases in both Abeta1-40 and Abeta1-42 were observed. Although adenosine A(1) or A(2A) receptor densities in cortex or hippocampus were not affected by caffeine treatment, brain adenosine levels in Tg mice were restored back to normal by dietary caffeine and could be involved in the cognitive protection provided by caffeine. Our data demonstrate that moderate daily intake of caffeine may delay or reduce the risk of AD.
PMID: 16938404

The complete paper to the above abstract can be found at --

When they refer to "adenosine", I wonder if they mean ATP.  See Mitochondrial Dysfunction for more on this.

The Caffeine Study
Press Release --

Caffeine reverses memory impairment in Alzheimer's mice
New studies show caffeine markedly reduced the hallmark protein for Alzheimer's disease in the brains and blood of the mice


Caffeine testing:

http://www.springwise.com/food_beverage/caffeine_test_strips_reveal_th/ [NO LONGER IN PRODUCTION!!!]

That Caffeine in Your Drink -- Is It Really 'Natural?'
ScienceDaily (Mar. 7, 2012)


More notes:

Caffeine stabilizes mitochondria by modulating tau phosphorylation and affecting Akt signaling in post mitotic neurons (Currais, Kato, et al 2011).
Abstract at: http://www.ncbi.nlm.nih.gov/pubmed/20838929

Caffeine also suppresses glycogen synthase kinase (GSK)-3αGSK-3β, a key stimulator of neurofibrillary tangle (NFT) formation, in the Arendash & Cao study (2010).
Abstract at: http://www.ncbi.nlm.nih.gov/pubmed/20182037

The Journal of Alzheimer's Disease devoted a whole supplement(22 articles) to the therapeutic properties of coffee: http://iospress.metapress.com/content/t13614762731/?p=b8fb38246a8c412289a907dd44be3382&pi=80

Known sources:

Natural sources:

Caffeine suppresses amyloid-beta levels in plasma and brain of Alzheimer's disease transgenic mice.
Cao C, Cirrito JR, Lin X, Wang L, Verges DK, Dickson A, Mamcarz M, Zhang C, Mori T, Arendash GW, Holtzman DM, Potter H.
J Alzheimers Dis. 2009;17(3):681-97.
Source: The Byrd Alzheimer's Center & Research Institute, Tampa, FL, USA.

Erratum in J Alzheimers Dis. 2009 Nov;18(3):727. Wang, Lilly [corrected to Wang, Li]..

Recent epidemiologic studies suggest that caffeine may be protective against Alzheimer's disease (AD). Supportive of this premise, our previous studies have shown that moderate caffeine administration protects/restores cognitive function and suppresses brain amyloid-beta (Abeta) production in AD transgenic mice. In the present study, we report that acute caffeine administration to both young adult and aged AD transgenic mice rapidly reduces Abeta levels in both brain interstitial fluid and plasma without affecting Abeta elimination. Long-term oral caffeine treatment to aged AD mice provided not only sustained reductions in plasma Abeta, but also decreases in both soluble and deposited Abeta in hippocampus and cortex. Irrespective of caffeine treatment, plasma Abeta levels did not correlate with brain Abeta levels or with cognitive performance in individual aged AD mice. Although higher plasma caffeine levels were strongly associated with lower plasma Abeta1-40 levels in aged AD mice, plasma caffeine levels were also not linked to cognitive performance. Plasma caffeine and theophylline levels were tightly correlated, both being associated with reduced inflammatory cytokine levels in hippocampus. Our conclusion is two-fold: first, that both plasma and brain Abeta levels are reduced by acute or chronic caffeine administration in several AD transgenic lines and ages, indicating a therapeutic value of caffeine against AD; and second, that plasma Abeta levels are not an accurate index of brain Abeta levels/deposition or cognitive performance in aged AD mice.
PMID: 19581723 [PubMed]



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Updated: July 2, 2012
Inception: July 2, 2012