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Sci Rep. 2017 Apr 27;7(1):1225. doi: 10.1038/s41598-017-01327-w.

Decreased body mass index in the preclinical stage of autosomal dominant Alzheimer's disease.

Author information

1
Department of Psychiatry and Psychotherapy, University of Tübingen, 72076, Tübingen, Germany.
2
German Center for Neurodegenerative Diseases (DZNE), 72076, Tübingen, Germany.
3
Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, Perth, WA, 6027, Australia.
4
School of Psychiatry and Clinical Neurosciences, University of Western Australia, Nedlands, WA, 6009, Australia.
5
Section for Dementia Research, Department of Cellular Neurology, Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy, University of Tübingen, 72076, Tübingen, Germany.
6
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076, Tübingen, Germany.
7
Memory and Aging Center, Keck School of Medicine of USC, Los Angeles, CA, USA.
8
University of Pittsburgh School of Medicine, Department of Neurology, 3471 5th Ave, Suite 811, Pittsburgh, PA, 15213, USA.
9
Neuroscience Research Australia, Randwick, Sydney, NSW, 2031, Australia.
10
School of Medical Sciences, University of New South Wales, Sydney, NSW, 2052, Australia.
11
Department of Pathology and Laboratory Medicine, Indiana University, Indianapolis, IN, 46202, USA.
12
Dementia Research Centre, Department of Neurodegeneration, UCL Institute of Neurology, Queen Square, London, WC1 3BG, UK.
13
Department of Neuroscience, Mayo Clinic, Jacksonville, Florida and Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA.
14
German Center for Neurodegenerative Diseases (DZNE), München, Germany and Department of Neurology, Ludwig-Maximilians Universität Munich, Munich, Germany.
15
Shiley-Marcos Alzheimer's Disease Research Center, Department of Neurosciences, University of California, San Diego, CA, USA.
16
Indiana University Center for Bioethics, 410 West 10th Street, Indianapolis, IN, 46202, USA.
17
Department of Neurology, The Warren Alpert Medical School of Brown University, Providence, RI, USA.
18
Division of Biostatistics, The Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St Louis, MO, USA.
19
Department of Neurology, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, 63108, USA.
20
Mental Health Research Institute, University of Melbourne, Level 5, Kenneth Myer Building, 30 Royal Parade, Parkville, Victoria, 3010, Australia.
21
Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
22
German Center for Neurodegenerative Diseases (DZNE), 72076, Tübingen, Germany. christoph.laske@med.uni-tuebingen.de.
23
Section for Dementia Research, Department of Cellular Neurology, Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy, University of Tübingen, 72076, Tübingen, Germany. christoph.laske@med.uni-tuebingen.de.

Abstract

The relationship between body-mass index (BMI) and Alzheimer´s disease (AD) has been extensively investigated. However, BMI alterations in preclinical individuals with autosomal dominant AD (ADAD) have not yet been investigated. We analyzed cross-sectional data from 230 asymptomatic members of families with ADAD participating in the Dominantly Inherited Alzheimer Network (DIAN) study including 120 preclinical mutation carriers (MCs) and 110 asymptomatic non-carriers (NCs). Differences in BMI and their relation with cerebral amyloid load and episodic memory as a function of estimated years to symptom onset (EYO) were analyzed. Preclinical MCs showed significantly lower BMIs compared to NCs, starting 11.2 years before expected symptom onset. However, the BMI curves begun to diverge already at 17.8 years before expected symptom onset. Lower BMI in preclinical MCs was significantly associated with less years before estimated symptom onset, higher global Aβ brain burden, and with lower delayed total recall scores in the logical memory test. The study provides cross-sectional evidence that weight loss starts one to two decades before expected symptom onset of ADAD. Our findings point toward a link between the pathophysiology of ADAD and disturbance of weight control mechanisms. Longitudinal follow-up studies are warranted to investigate BMI changes over time.

PMID:
28450713
PMCID:
PMC5430642
DOI:
10.1038/s41598-017-01327-w
[Indexed for MEDLINE]
Free PMC Article

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