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.

Original languageEnglish
Pages (from-to)75
JournalAlzheimer's Research & Therapy
Volume10
Issue number1
DOIs
Publication statusPublished - 4 Aug 2018

Cite this

@article{5aea7edef59d4f489292df6a93f690f6,
title = "The EMIF-AD PreclinAD study: study design and baseline cohort overview",
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.",
author = "Elles Konijnenberg and Carter, {Stephen F} and {Ten Kate}, Mara and {den Braber}, Anouk and Jori Tomassen and Chinenye Amadi and Linda Wesselman and Hoang-Ton Nguyen and {van de Kreeke}, {Jacoba A} and Maqsood Yaqub and Matteo Demuru and Mulder, {Sandra D} and Arjan Hillebrand and Bouwman, {Femke H} and Teunissen, {Charlotte E} and Sern{\'e}, {Erik H} and Moll, {Annette C} and Verbraak, {Frank D} and Rainer Hinz and Neil Pendleton and Lammertsma, {Adriaan A} and {van Berckel}, {Bart N M} and Frederik Barkhof and Boomsma, {Dorret I} and Philip Scheltens and Karl Herholz and Visser, {Pieter Jelle}",
year = "2018",
month = "8",
day = "4",
doi = "10.1186/s13195-018-0406-7",
language = "English",
volume = "10",
pages = "75",
journal = "Alzheimer's Research & Therapy",
issn = "1758-9193",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - The EMIF-AD PreclinAD study

T2 - study design and baseline cohort overview

AU - Konijnenberg, Elles

AU - Carter, Stephen F

AU - Ten Kate, Mara

AU - den Braber, Anouk

AU - Tomassen, Jori

AU - Amadi, Chinenye

AU - Wesselman, Linda

AU - Nguyen, Hoang-Ton

AU - van de Kreeke, Jacoba A

AU - Yaqub, Maqsood

AU - Demuru, Matteo

AU - Mulder, Sandra D

AU - Hillebrand, Arjan

AU - Bouwman, Femke H

AU - Teunissen, Charlotte E

AU - Serné, Erik H

AU - Moll, Annette C

AU - Verbraak, Frank D

AU - Hinz, Rainer

AU - Pendleton, Neil

AU - Lammertsma, Adriaan A

AU - van Berckel, Bart N M

AU - Barkhof, Frederik

AU - Boomsma, Dorret I

AU - Scheltens, Philip

AU - Herholz, Karl

AU - Visser, Pieter Jelle

PY - 2018/8/4

Y1 - 2018/8/4

N2 - 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.

AB - 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.

U2 - 10.1186/s13195-018-0406-7

DO - 10.1186/s13195-018-0406-7

M3 - Article

VL - 10

SP - 75

JO - Alzheimer's Research & Therapy

JF - Alzheimer's Research & Therapy

SN - 1758-9193

IS - 1

ER -