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S44 Aging and Dementia: Imaging and Neuropathology
February 12, 2013
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Beta Blocker Treatment of Hypertensive Older Persons Ameliorates the Brain Lesions of Dementia Measured at Autopsy: The Honolulu-Asia Aging Study (S44.005)

February 12, 2013 issue
80 (7_supplement) S44.005

Abstract

OBJECTIVE: To examine the relationship to brain lesions at autopsy of treatment with a beta blocker, as compare with other drugs.
BACKGROUND: The HAAS is a community-based study of Japanese-American men aged 71-93 at baseline, conducted 1991-2012. Prior analyses identified elevated midlife blood pressure as a risk factor for Alzheimer's disease, cognitive impairment, and Alzheimer brain lesions at autopsy. Midlife systolic pressure >120mm Hg was a predictor for 17-27% (population attributable risk) of subsequent dementia cases. While angiotensin receptor blockers and other treatments have been reported to reduce the development of dementia, comparisons with beta blockers are lacking. A concurrent analysis in HAAS subjects demonstrates a congruent amelioration of cognitive decline or impairment associated with beta blocker use, including but not limited to participants described in this report.
DESIGN/METHODS: Of 774 autopsied men, 610 had been hypertensive or treated with anti-hypertensive drugs. Logistic and linear regression analyses took into account non-normal neuropathologic endpoint distributions while adjusting for age, baseline pressures and cognitive test score, follow-up interval, age at death, diabetes, apolipoprotein E genotype, midlife hypertension and treatment thereof.
RESULTS: Autopsied HAAS subjects treated with beta blockers as the sole medication were found to have significantly fewer microinfarcts, less brain atrophy, and fewer Alzheimer brain lesions compared with decedents who had received other medications. Those who had received beta blockers plus other medications had intermediate or marginally fewer brain abnormalities.
CONCLUSIONS: Compared with other treatments, beta blocker use in HAAS participants was associated with lower levels of neuropathologic abnormalities associated with cognitive impairment and dementia.
Supported by: NIH grants UO-1 AG09349 and UO-1 AG017155.
Disclosure: Dr. White has nothing to disclose. Dr. Gelber has nothing to disclose. Dr. Launer has nothing to disclose. Dr. Zarow has nothing to disclose. Dr. Sonnen has nothing to disclose. Dr. Uyehara-Lock has nothing to disclose. Dr. Masaki has nothing to disclose. Dr. Ross has received research support from the Michael J. Fox Foundation. Dr. Petrovitch has nothing to disclose.

Information & Authors

Information

Published In

Neurology®
Volume 80Number 7_supplementFebruary 12, 2013
Pages: S44.005

Publication History

Published online: February 12, 2013
Published in issue: February 12, 2013

Notes

Thursday, March 21 2013, 12:00 pm-2:00 pm

Authors

Affiliations & Disclosures

Lon White
neuroepidemiology Pacific Health Research and Education Institute Honolulu HI
Rebecca Gelber
Research Hawaii Dept of Veterans Affairs Honolulu HI
Lenore Launer
Lab of Epidemiology, Demography, and Biometry Natiional Institutie on Aging, NIH Washington DC
Chris Zarow
Neurology University of Southern California School of Medicine Downey CA
Joshua Sonnen
Pathology University of Washington School of Medicine Seattle WA
Jane Uyehara-Lock
Pathology John A Burns School of Medicine, University of Hawaii Honolulu HI
Kamal Masaki
geriatric medicine John A Burns School of Medicine, University of Hawaii Honolulu HI
George Ross
Research Hawaii Dept of Veterans Affairs Honolulu HI
Helen Petrovitch
research Pacific Health Research and Education Institute Honolulu HI

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Cited By
  1. Preventing Vascular Effects on Brain Injury and Cognition Late in Life: Knowns and Unknowns, Neuropsychology Review, 24, 3, (371-387), (2014).https://doi.org/10.1007/s11065-014-9264-7
    Crossref
  2. Degenerative Brain Diseases and White Matter Injury, White Matter Injury in Stroke and CNS Disease, (281-319), (2013).https://doi.org/10.1007/978-1-4614-9123-1_14
    Crossref
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