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When citing an abstract from the 2009 Annual - Society for ...

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Poster<br />

529. Treatments: Alzheimer's <strong>an</strong>d Neurodegeneration<br />

Location: South Hall A<br />

Time: Tuesday, October 20, <strong>2009</strong>, 8:00 am - 12:00 noon<br />

Program#/Poster#: 529.3/I28<br />

Topic: C.02.o. Therapies<br />

Support: ADRC gr<strong>an</strong>t P50AG025711<br />

Funds <strong>from</strong> <strong>the</strong> Byrd Institute<br />

Title: The <strong>the</strong>rapeutic effects of caffeine <strong>an</strong>d coffee in Alzheimer’s disease<br />

Authors: *C. CAO 1 , X. LIN 1 , L. WANG 2 , M. MAMCARZ 2 , M. RUNFELDT 1 , G. W.<br />

ARENDASH 2 ;<br />

1 Mol. Pharmacol. <strong>an</strong>d Physiol., 2 Biol., Univ. of South Florida, Tampa, FL<br />

Abstract: The premise that caffeine/coffee may provide a safe, effective, readily available, <strong>an</strong>d<br />

inexpensive <strong>the</strong>rapeutic against Alzheimer’s Disease (AD) is underscored by a growing body of<br />

epidemiologic literature showing protective effects against memory impairment <strong>an</strong>d AD. For<br />

example, mid-life coffee consumption has been linked to a 65% decreased risk of AD. Our own<br />

work in AD tr<strong>an</strong>sgenic mice has shown that caffeine both protects against <strong>an</strong>d reverses cognitive<br />

impairment by directly affecting Aβ pathogenesis. To determine <strong>the</strong> extent to which noncaffeinergic<br />

components of coffee may be involved in <strong>the</strong> cognitive benefits of coffee, we have<br />

conducted a long-term study involving three months daily treatment by gavage with regular<br />

coffee or decaffeinated coffee to APP/PS1 (Tg) mice. Both coffee <strong>an</strong>d decaffeinated coffee were<br />

prepared in <strong>the</strong> same way <strong>an</strong>d <strong>the</strong> caffeine concentration of each was measured be<strong>for</strong>e<br />

administrated. Behavior testing near <strong>the</strong> end of <strong>the</strong> treatment period revealed that coffee treated<br />

Tg mice had signific<strong>an</strong>tly improved working memory compared to control Tg mice. By contrast,<br />

<strong>the</strong> decaffeinated coffee treatment group of Tg mice exhibited no such beneficial effects. Plasma<br />

cytokine <strong>an</strong>alysis none<strong>the</strong>less indicated that both caffeine <strong>an</strong>d non-caffeinergic compounds in<br />

coffee c<strong>an</strong> provide beneficial effects <strong>an</strong>d act synergistically. We also <strong>an</strong>alyzed 208 hum<strong>an</strong><br />

plasma samples <strong>for</strong> caffeine levels <strong>from</strong> two clinical sites of <strong>the</strong> Florida Alzheimer’s Disease<br />

Research Center (119 <strong>from</strong> Miami <strong>an</strong>d 89 <strong>from</strong> Tampa), divided into AD, MCI <strong>an</strong>d normal aged<br />

individuals. Our result show that spont<strong>an</strong>eous caffeine levels in normal aged subject are<br />

signific<strong>an</strong>tly higher th<strong>an</strong> AD subjects at <strong>the</strong> Tampa site, but no signific<strong>an</strong>t difference compared<br />

with MCI, while caffeine levels in normal is higher th<strong>an</strong> MCI <strong>an</strong>d AD in subjects at <strong>the</strong> Miami<br />

site. Thus, our results <strong>from</strong> both <strong>an</strong>imal studies <strong>an</strong>d hum<strong>an</strong> habitual caffeine intake show a<br />

consistent association of caffeine with normal or maintained cognitive function. Additionally, in

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