BIO

Bernard Hanseeuw is a behavioral neurologist conducting research on early Alzheimer’s disease with the aim of better caring for patients with or at-risk for memory decline. He graduated as an MD (2007), PhD (2012), and board certification in Neurology (2014) from Université Catholique de Louvain (Belgium). He then completed a post-doctoral research fellowship in Reisa Sperling’s and Keith Johnson’s lab at Harvard Medical School (Boston, MA, USA) from 2014 to 2017. 
Bernard Hanseeuw is the Co-Director of the Memory Clinic at Saint-Luc University Hospital (Brussels, Belgium) and the president of the Belgian Neurological Society (2024-2025). He holds the position of Instructor at the Gordon Center for Medical Imaging (Harvard Medical School). His research is supported by the Belgian National Fund for Scientific Research (FNRS/WelBio) and the Belgian Foundation for Alzheimer’s Research. His main research interests lies in the longitudinal assessment of amyloid and tau pathologies in clinically normal and mildly impaired older adults using both neuroimaging and bio-fluid analyses. Dr. Hanseeuw is site-PI for many AD clinical trials, including prevention trials in preclinical AD, and a member of the executive committee of AMYPAD, a European consortium collecting amyloid imaging to prevent Alzheimer’s disease.

His publication list can be found at: 
https://www.ncbi.nlm.nih.gov/pubmed/?term=hanseeuw
If you like TEDx talks, please enjoy this show:
https://www.youtube.com/watch?v=WQvfNG9bkz0

ABSTRACT

Until a decade ago, a definite diagnosis of Alzheimer’s disease (AD) could only be made after autopsy and confirmation of amyloid and tau pathology in the brain. Neurologists could only give the diagnosis of probable AD to patients with dementia. The absence of biomarkers to confirm the biological diagnosis made it impossible to diagnose AD early, prior to dementia. The Louvain Aging Brain Lab has been among the first in Europe to describe the spatio-temporal progression of Alzheimer’s pathology in living humans, using specific radiotracers and positron emission tomography to detect amyloid and tau deposits in the brain. We have “brought to life” neuropathological classifications, obtained at post-mortem, by transposing them into brain imaging classifications, applicable to detect Alzheimer’s pathology before the onset of symptoms. It appeared that amyloid PET was able to predict which patient would progress to dementia six years later with an overall predictive value of 87%. However, regional amyloid did not predict well the specific cognitive deficits, and up to 20% of cognitively normal older adults do have amyloid pathology in their brain. In contrast, tau PET images (see figure) are much more closely associated to brain dysfunction and cognitive deficits. We are currently developing new ways of assessing subtle cognitive loss, including spatial navigation or linguistic abilities, in apparently normal older adults. This work is of particular importance in the context of upcoming therapeutic trials aiming at preventing the onset of AD in non-demented individuals with evidence of Alzheimer’s pathology. The recent development of blood tests targeting amyloid and tau, of cognitive tests available on smartphone apps, and the large amounts of data collected using brain imaging all require artificial intelligence tool to be analyzed optimally. 

Tau PET images in patients with different levels of Alzheimer’s pathology
Early stages (I-II) are commonly observed in older individuals, even without memory impairment. Stages III-IV are most often associated with mild cognitive impairment and late stages (V-VI) with dementia.