What we do
About our project
Objective
To study in a population-based setting, in persons free of dementia, the interplay between amyloid-β pathology and vascular pathology. We hypothesize that higher overall load and progression of vascular pathology will relate to a higher burden of amyloid-β pathology; and that both pathologies interact in their effect on (decline in) cognitive functioning. As a secondary objective we will furthermore examine whether Apolipoprotein E4 (APOE4) affects these relations.
Study design
In a sample of 700 persons from the Rotterdam Study aged 60 or above, brain amyloid PET imaging will be acquired. To ensure a good representation of different stages of vascular brain pathology, these 700 participants will be selected by random sampling from quartiles of the distribution of white matter lesion volume load, as quantified on previous brain MRI.
Clinical relevance
This study is particularly relevant as vascular factors are potentially modifiable and thus could prove preventive targets for Alzheimer’s disease, especially when shown to modify amyloid-β pathology.
Our research focus
Population-based setting
This study will make use of the existing infrastructure within The Rotterdam Study, a large on-going population-based study with extensive multiple time-point data in different research areas, including neurological and cardiovascular diseases. The use of brain magnetic resonance imaging within the Rotterdam Study, enables a detailed assessment of vascular pathology. With our research, we’d like to add the assessment of amyloid-β pathology to this large population-based cohort to assess possible interactions with vascular pathology.
Focus on interaction
Central to the quest for the etiology of Alzheimer’s disease is insight into how the two prevailing pathways, amyloid-β pathology and vascular pathology, influence disease development in its earliest stage. These pathways could act as independent processes leading to dementia, or alternatively, they may directly influence each other, interact and cause an accelerated disease process. Evidence from the two pathways influencing each other comes from both experimental studies and patient-based studies. Yet, there is a void of studies that use an integrated approach to study both pathways simultaneously, in particular in a preclinical setting.
Funds & Grants
Life Molecular Imaging, tracer sponsoring, www.life-mi.com
Collaborations
The department of Radiology & Nuclear Medicine
The department of Epidemiology
Outside Erasmus MC
Life Molecular Imaging, www.life-mi-.com
Our team
Meike Vernooij
Danielle van Assema
Rebecca Steketee
Joyce van Arendonk
Julia Neitzel
