Thursday, July 9th, 2009...10:56 am

Caffeine and Alzheimer’s Disease – The Abstract

By: Michael Allen Smith

It now appears my original source for the caffeine and Alzheimer’s Disease story wasn’t the best.  The Times UK reported that caffeine could delay the effects of AD, whereas the BBC report stated it could reverse the effects.  That is a huge difference in reporting.  Which is it?

I decided to do something I should have done first.  I went directly to the source and read the abstract.  Ever notice how the major media never links to the academic sources they cite in their stories?  If you are reporting on a study in the Journal of Alzheimer’s Disease and they have a web presence, link to them.

From the Journal of Alzheimer’s Disease Volume 17, Number 3, July 2009 Page 661-680:

Gary W. Arendash, Takashi Mori, Chuanhai Cao, Malgorzata Mamcarz, Melissa Runfeldt, Alexander Dickson, Kavon Rezai-Zadeh, Jun Tan, Bruce A. Citron, Xiaoyang Lin, Valentina Echeverria, Huntington Potter

Caffeine Reverses Cognitive Impairment and Decreases Brain Amyloid-β Levels in Aged Alzheimer’s Disease Mice

Abstract: We have recently shown that Alzheimer’s disease (AD) transgenic mice given a moderate level of caffeine intake (the human equivalent of 5 cups of coffee per day) are protected from development of otherwise certain cognitive impairment and have decreased hippocampal amyloid-β (Aβ) levels due to suppression of both β-secretase (BACE1) and presenilin 1 (PS1)/g-secretase expression. To determine if caffeine intake can have beneficial effects in “aged” APPsw mice already demonstrating cognitive impairment, we administered caffeine in the drinking water of 18-19 month old APPsw mice that were impaired in working memory. At 4-5 weeks into caffeine treatment, those impaired transgenic mice given caffeine (Tg/Caff) exhibited vastly superior working memory compared to the continuing impairment of control transgenic mice. In addition, Tg/Caff mice had substantially reduced Aβ deposition in hippocampus (down 40%) and entorhinal cortex (down 46%), as well as correlated decreases in brain soluble Aβ levels. Mechanistically, evidence is provided that caffeine suppression of BACE1 involves the cRaf-1/NFκB pathway. We also determined that caffeine concentrations within human physiological range effectively reduce active and total glycogen synthase kinase 3 levels in SweAPP N2a cells. Even with pre-existing and substantial Aβ burden, aged APPsw mice exhibited memory restoration and reversal of AD pathology, suggesting a treatment potential of caffeine in cases of established AD.

Based off this abstract it appears that caffeine both prevents and reverses the effects characteristic of Alzheimer’s Disease. My guess is the next step will be to have other studies confirm these findings and if they hold true to then drill down what the optimal range of caffeine to be used for patients that have AD and the preventative dose for those at risk.

I’m not a scientist, but I do have a hunch that 500 mg of caffeine is high.   I also know a thing about caffeine tolerance and am curious if that ends up playing a role.  Some people can not handle caffeine even in the smallest doses. Those of us that can handle higher doses of caffeine, got to super human caffeine junkie status through years of training. Going from 0 mg to 500 mg is a crazy leap. Also note that coffee and tea are calorie free and loaded with antioxidants. Colas are loaded with sugar or artificial sweeteners and are nutrient deficient.  If you or a loved one is considering joining Camp Caffeine, there is a healthier path.

Source:

Journal of Alzheimer’s Disease – Volume 17, Number 3, July 2009 Page 661-680

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