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Am J Geriatr Psychiatry. 2016 Sep;24(9):729-37. doi: 10.1016/j.jagp.2016.05.007. Epub 2016 May 13.

Modifiable Risk Factors and Brain Positron Emission Tomography Measures of Amyloid and Tau in Nondemented Adults with Memory Complaints.

Author information

1
Division of Geriatric Psychiatry, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience & Human Behavior, David Geffen School of Medicine, and Longevity Center, University of California, Los Angeles, CA. Electronic address: dmerrill@mednet.ucla.edu.
2
Division of Geriatric Psychiatry, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience & Human Behavior, David Geffen School of Medicine, and Longevity Center, University of California, Los Angeles, CA.
3
Department of Radiology, UCLA Health System, David Geffen School of Medicine, University of California, Los Angeles, CA.
4
Center for Cognitive Neurosciences, Semel Institute for Neuroscience & Human Behavior, University of California, Los Angeles, CA.
5
Department of Molecular and Medical Pharmacology, Center for Health Sciences, University of California, Los Angeles, CA.

Abstract

OBJECTIVE:

Exercise and diet impact body composition, but their age-related brain effects are unclear at the molecular imaging level. To address these issues, the authors determined whether body mass index (BMI), physical activity, and diet relate to brain positron emission tomography (PET) of amyloid plaques and tau tangles using 2-(1-(6-[(2-[F-18]fluoroethyl)(methyl)amino]-2-naphthyl)ethylidene)malononitrile (FDDNP).

METHODS:

Volunteers (N = 44; mean age: 62.6 ± 10.7 years) with subjective memory impairment (N = 24) or mild cognitive impairment (MCI; N = 20) were recruited by soliciting for memory complaints. Levels of physical activity and extent of following a Mediterranean-type diet were self-reported. FDDNP-PET scans assessed plaque/tangle binding in Alzheimer disease-associated regions (frontal, parietal, medial and lateral temporal, posterior cingulate). Mixed models controlling for known covariates examined BMI, physical activity, and diet in relation to FDDNP-PET.

RESULTS:

MCI subjects with above normal BMI (>25) had higher FDDNP-PET binding compared with those with normal BMI (1.11(0.03) versus 1.08(0.03), ES = 1.04, t(35) = 3.3, p = 0.002). Greater physical activity was associated with lower FDDNP-PET binding in MCI subjects (1.07(0.03) versus 1.11(0.03), ES = 1.13, t(35) = -3.1, p = 0.004) but not in subjects with subjective memory impairment (1.07(0.03) versus 1.07(0.03), ES = 0.02, t(35) = -0.1, p = 0.9). Healthier diet related to lower FDDNP-PET binding, regardless of cognitive status (1.07(0.03) versus 1.09(0.02), ES = 0.72, t(35) = -2.1, p = 0.04).

CONCLUSION:

These preliminary findings are consistent with a relationship between risk modifiersand brain plaque/tangle deposition in nondemented individuals and supports maintenance of normal body weight, regular physical activity, and healthy diet to protect the brain during aging. (clinicaltrials.gov; NCT00355498).

KEYWORDS:

Alzheimer disease; FDDNP; PET; exercise

PMID:
27421618
PMCID:
PMC5003686
DOI:
10.1016/j.jagp.2016.05.007
[Indexed for MEDLINE]
Free PMC Article

Conflict of interest statement

Financial Disclosures: Dr. Merrill reports having received lecture fees from Assurex Health. Dr. Barrio and Dr. Small co-inventors of FDDNP-PET, which UCLA has licensed to TauMark, LLC. Dr. Barrio and Dr. Small have a financial interest in TauMark, LLC. Dr. Small reports having served as a consultant and/or having received lecture fees from Novartis, Forum Pharmaceuticals, Lily and Herbalife; grants from POM Wonderful; and writing fees from Herbalife, Newsmax Media, and Workman Publishing. Dr. Lavretsky reports having received grant support from Forest Research Institute and the Alzheimer’s Research and Prevention Foundation and consulting fees from Eli Lilly. Drs. Siddarth, Raji, Ercoli, Miller, Harris, Burggren, Bookheimer, Mrs. Emerson, and Ms. Rueda have no financial conflicts of interest.

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