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A BSTRACTS
trolling for resident demographics, acuity, and facility characteristics,
there was a 2.8% (Standard Error 0.01; p=0.004) increase in death at
30 days and a 3.9% (Standard Error 0.01; p=0.008) increase in death
at 90 days for residents with severe dementia who evacuated for Hurricane
Gustav.
Conclusions: Nationwide, of the approximately 1.6 million
adults who live in nursing homes, an estimated 50% to 70% carry a
diagnosis of Alzheimer’s disease or a related dementia. This research
reveals the deleterious effects of evacuation on residents
with severe dementia. Interventions need to be developed and
tested to determine the best methods for protecting this at-risk
population when there are no other options than to evacuate the
facility.
B122
Proteinuria in Mid-Life and Cognitive Function in Late-Life: The
Honolulu-Asia Aging Study.
M. Higuchi, 1 R. Chen, 2 C. Bell, 1 L. Wongvarcharoen, 1 W. Ross, 3,1
H. Petrovitch, 1,2 L. Launer, 4 R. Abbott, 1 K. Masaki. 1,2 1. Geriatric
Medicine, University of Hawaii, Honolulu, HI; 2. Kuakini Medical
Center, Honolulu, HI; 3. VA Pacific Islands Healthcare System,
Honolulu, HI; 4. National Institute on Aging, Bethesda, MD.
Supported By: The National Heart, Lung, and Blood Institute; the
National Institute on Aging; Veterans Affairs Pacific Islands
Healthcare Systems; John A. Hartford Foundation Center of
Excellence in Geriatrics, University of Hawaii.
Background: Impairment of renal function has been linked to
cognitive impairment. There are few longitudinal studies of proteinuria
and cognitive function. We assessed mid-life proteinuria and
cognitive decline or incident dementia in an elderly Asian male population.
Methods: The Honolulu Heart Program (HHP) is a prospective
study that began in 1965 with 8,006 Japanese-American men ages 45-
68 years. Mid-life proteinuria was detected by urine dipstick at exam
3 (1971-74). Subjects were classified into 3 groups: no proteinuria,
trace, and positive. The Honolulu-Asia Aging Study of dementia
began 20 years later with HHP exam 4 (1991-93) with 3,734 men ages
71-93 years. Global cognitive function was assessed by the Cognitive
Abilities Screening Instrument (CASI) (score range 0-100). Cognitive
decline was defined as drop in CASI score of >=1 SD (>=10
points at 3 years, >=14 at 6 years, >=14 at 8 years). Standard criteria
were used to classify 8-year incident dementia (DSM-IIIR),
Alzheimer’s Disease (NINDS-ADRDA), and Vascular Dementia
(California ADDTC).
Results: No proteinuria was found in 97.2% of subjects, trace in
1.7% and positive proteinuria in 1.1%. Age-adjusted incident dementia
rates increased significantly from 13.8, to 22.8, to 39.7 per 1,000
person years follow-up, among those with no, trace and positive proteinuria
respectively, p=0.004. Using multiple logistic regression adjusting
for age, education, apoE4, prevalent stroke, hypertension, diabetes,
and baseline CASI, those with positive proteinuria were more
likely to have cognitive decline (3-year decline OR=2.89, 95%
CI=1.28-6.55, p=0.011; 6-year decline OR=3.46, 95% CI=1.15-10.4,
p=0.027; 8-year decline OR=3.74, 95% CI=1.15-12.1, p=0.028), using
no proteinuria as reference. Multivariate Cox regression found a significant
association between positive proteinuria and all-cause incident
dementia (RR=2.71, 95% CI=1.20-6.09, p=0.016) and incident
Vascular Dementia (RR= 6.38, 95%CI=1.98-20.5, p=0.002), using no
proteinuria as reference.
Conclusion: Proteinuria in mid-life was an independent predictor
for late-life incident dementia and cognitive decline over 8
years. This association needs to be confirmed in other ethnic groups
and women.
B123
Effect of rapamycin in a mouse model of synucleinopathy.
M. Hughes, 1 M. Wey, 2 X. Bai, 2 A. Martinez, 2 E. Fernandez, 2,3
R. Strong. 2,3 1. School of Medicine, UTHSCSA, San Antonio, TX; 2.
Pharmacology, Barshop Institute for Longevity and Aging Studies,
San Antonio, TX; 3. Geriatric Research, Education and Clinical
Center, South Texas Veterans Health Care Network, San Antonio, TX.
Supported By: MH was supported by the MSTAR program, the
American Federation for Aging Research and the NIA. Support for
this project also included PHS grants AG022307, AG036613 and
AG13319 and by a grant from the Department of Veterans Affairs
Medical Research Program (RS).
Background: Synucleinopathies, including Parkinson’s disease
(PD), multiple system atrophy and the Lewy body variant of
Alzheimer’s disease (AD), are age-related neurodegenerative disorders
characterized by expression of pathological intracellular inclusions
containing α-synuclein. Mice transgenic for α-synuclein containing
the human A53T mutation, expressed specifically in neurons,
exhibit severe motor symptoms. Rapamycin has been shown to be
neuroprotective in mouse models of several neurodegenerative disorders,
including AD, Huntington’s disease and PD. However, it was
unknown whether rapamycin would be effective in an animal model
of synucleinopathy. The aim of this study was to determine whether
rapamycin reduces accumulation of α-synuclein and attenuates
motor deficits in A53T transgenic mice.
Methods: Mouse diet containing microencapsulated rapamycin
(14 ppm in diet; 2.25 mg/kg body weight/day) was fed to age-matched
wild type and A53T transgenic mice from 13 to 41 weeks of age. The
control diet contained the microencapsulation material. The mice
were assessed on several tests of motor performance including the
pole test, forepaw stepping adjustment test, accelerating rotarod, grip
strength test, gait performance and the challenging beam traversal
test. Expression of α-synuclein in midbrain, striatum, cerebellum, and
spinal cord was tested by Western analysis.
Results: Rapamycin significantly improved performance on the
forepaw stepping adjustment test, the rotarod and the pole test in
both genders of transgenic mice. Rapamycin significantly reduced
error steps on the challenging beam traversal test in male, but not female,
transgenic mice. Feeding rapamycin had no effect on grip
strength or stride length or any effect in wild-type mice. Rapamycin
significantly reduced expression of human α-synuclein in midbrain
and spinal cord, but not in striatum or cerebellum.
Conclusions: Rapamycin significantly attenuated motor deficits
in the A53T mice by reducing human α-synuclein expression in midbrain
and spinal cord. Further experiments will determine whether
the effect of rapamycin is through enhancement of autophagy and
whether rapamycin prevents neurodegeneration.
B124
Does Slow Reaction Time Predict Incident Parkinson’s Disease?:
The Honolulu-Asia Aging Study.
M. Inaba, 1 M. Kamal, 1,2 R. D. Abbott, 1 K. Fong, 2 C. Bell, 1
H. Petrovitch, 1,2 C. Tanner, 4 W. G. Ross. 3,1 1. Geriatric Medicine,
University of Hawaii, Honolulu, HI; 2. Kuakini Medical Center,
Honolulu, HI; 3. Veterans Affairs Pacific Islands Healthcare System,
Honolulu, HI; 4. The Parkinson’s Institute, Sunnyvale, CA.
Supported By: National Parkinson Foundation; the National
Institute on Aging; Veterans Affairs Pacific Islands Healthcare
Systems; John A. Hartford Foundation Center of Excellence in
Geriatrics, University of Hawaii.
Introduction: Many studies have shown a deficit in reaction time
(RT) in Parkinson’s disease (PD) patients. To date, there have been
no longitudinal population-based studies of RT and incident PD. We
studied whether RT may identify individuals at risk for PD among
elderly Japanese-American men.
AGS 2012 ANNUAL MEETING
S115