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[Abstract Title]. - Society for Neuroscience

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of the regional cerebral metabolic rate <strong>for</strong> glucose (CMRgl) as a presymptomatic quantitative<br />

endophenotype to evaluate putative genetic and non-genetic risk factors <strong>for</strong> AD.<br />

Objective: To test the hypothesis that hypertension is associated with lower CMRgl in brain<br />

regions affected by AD or normal aging. Secondly, examine whether higher higher systolic<br />

blood pressure (SBP) and diastolic blood pressure (DBP) are inversely correlated with CMRgl in<br />

these brain regions.<br />

Methods: A brain mapping algorithm (SPM5) was used to characterize respective relationships<br />

between higher SBP, higher DBP, and hypertension and lower CMRgl in 26 cognitively normal<br />

persons (mean Mini-Mental State Examination [MMSE] score 29.4 ± 1.1) 60.6 ± 6.7 years of<br />

age, including 6 apolipoprotein E (APOE) ε4 homozgotes (HM), 11 heterozygotes (HT), and 9<br />

noncarriers (NC).<br />

Results: Participants with and without hypertension did not differ significantly in their age,<br />

gender, educational level or MMSE scores. Participants with hypertension had lower CMRgl<br />

than those who did not in parietal regions previously associated with AD and in frontal regions<br />

previously associated with AD and normal aging (p < 0.05 corrected <strong>for</strong> multiple comparisons).<br />

Similarly, higher SBP and DBP were each associated with lower CMRgl in temporal regions<br />

previously associated with AD and in frontal regions previously associated with normal aging (p<br />

< 0.005 uncorrected <strong>for</strong> multiple comparisons).<br />

Conclusions: These preliminary brain-imaging findings provide additional evidence that<br />

hypertension along with higher SBP and DBP are associated with an increased risk of AD. This<br />

study provides a foundation <strong>for</strong> using FDG PET to rapidly evaluate the efficacy of antihypertensive<br />

treatments in the primary prevention of AD.<br />

Disclosures: J.B.S. Langbaum, None; K. Chen, None; W. Lee, None; C. Recshke, None; S.<br />

Reeder, None; D. Bandy, None; G.E. Alexander, None; R.J. Caselli, None; E.M. Reiman,<br />

None.<br />

Poster<br />

247. Parkinson's Disease Interventions: Animal and Clinical Models<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 247.1/R8<br />

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

Support: (M103KV010021-06K2201-02110) from BRC<br />

(R15-2006-020) from NCRC (ROK)<br />

<strong>Title</strong>: Novel functional role of oxi gene family during oxidative stress induced dopamine<br />

neuronal cell death

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