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Alzheimers Res Ther. 2018 Aug 4;10(1):75. doi: 10.1186/s13195-018-0406-7.

The EMIF-AD PreclinAD study: study design and baseline cohort overview.

Author information

1
Alzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands. e.konijnenberg@vumc.nl.
2
Wolfson Molecular Imaging Centre, Division of Neuroscience and Experimental Psychology, University of Manchester, Manchester, UK.
3
Alzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
4
Department of Biological Psychology, VU University, Neuroscience Amsterdam, Amsterdam, The Netherlands.
5
Department of Ophthalmology, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
6
Department of Radiology & Nuclear Medicine, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
7
Neurochemistry Laboratory, Department of Clinical Chemistry, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
8
Department of Clinical Neurophysiology, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
9
Department of Internal Medicine, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
10
Wolfson Molecular Imaging Centre, Division of Informatics, Imaging and Data Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Manchester, UK.
11
Institutes of Neurology & Healthcare Engineering, UCL, London, UK.
12
Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.

Abstract

BACKGROUND:

Amyloid pathology is the pathological hallmark in Alzheimer's disease (AD) and can precede clinical dementia by decades. So far it remains unclear how amyloid pathology leads to cognitive impairment and dementia. To design AD prevention trials it is key to include cognitively normal subjects at high risk for amyloid pathology and to find predictors of cognitive decline in these subjects. These goals can be accomplished by targeting twins, with additional benefits to identify genetic and environmental pathways for amyloid pathology, other AD biomarkers, and cognitive decline.

METHODS:

From December 2014 to October 2017 we enrolled cognitively normal participants aged 60 years and older from the ongoing Manchester and Newcastle Age and Cognitive Performance Research Cohort and the Netherlands Twins Register. In Manchester we included single individuals, and in Amsterdam monozygotic twin pairs. At baseline, participants completed neuropsychological tests and questionnaires, and underwent physical examination, blood sampling, ultrasound of the carotid arteries, structural and resting state functional brain magnetic resonance imaging, and dynamic amyloid positron emission tomography (PET) scanning with [18F]flutemetamol. In addition, the twin cohort underwent lumbar puncture for cerebrospinal fluid collection, buccal cell collection, magnetoencephalography, optical coherence tomography, and retinal imaging.

RESULTS:

We included 285 participants, who were on average 74.8 ± 9.7 years old, 64% female. Fifty-eight participants (22%) had an abnormal amyloid PET scan.

CONCLUSIONS:

A rich baseline dataset of cognitively normal elderly individuals has been established to estimate risk factors and biomarkers for amyloid pathology and future cognitive decline.

KEYWORDS:

Amyloid; Cognitively normal; Monozygotic twins; Preclinical Alzheimer’s disease; [18F]flutemetamol

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