Caffeine and Alzheimer's

[Swarfmaker]

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)...

http://www.sciencedaily.com/releases/2010/05/100517111937.htm
http://news.bbc.co.uk/2/hi/health/8132122.stm
http://iospress.metapress.com/content/t13614762731/

Neuroscience. 2006 Nov 3;142(4):941-52. Epub 2006 Aug 28.
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.

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 --
http://www.byrdinstitute.org/mediaroom/caffeine-study/Caffeine%20Paper.pdf

The Caffeine Study Press Release --
http://www.byrdinstitute.org/mediaroom/caffeine-study/caffeine%20press%20release%20FINAL.pdf

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
http://www.eurekalert.org/pub_releases/2009-07/uosf-crm070109.php

http://www.neurology.org/cgi/content/abstract/69/6/536
http://www.sciencedaily.com/releases/2009/01/090114200005.htm