Geert Jan Biessels is associate professor and his work focusus on diabetes mellitus and ageing-related accelerated cognitive decline. The interview gives an impression on his motivation and specific interest in the neuroscience field. Cognition and diabetes
Diabetes mellitus is known to be associated with vascular disease, but there’s more to this increasingly frequent metabolic disorder. Diabetes is also strongly associated with ageing-related accelerated cognitive decline, it accounts for roughly ten percent of the population attributable risk of dementia. In other words, one in ten dementia cases may be attributed to concomitant diabetes. Interestingly, since risk factors associated with diabetes – e.g. high blood pressure, dyslipidemia – are modifiable, this may offer opportunities in preventing dementia.
Thus runs the central argument in the High Potential grant neurologist Geert Jan Biessels was awarded by Utrecht University. Together with neuropsychologist Roy Kessels he received 1 million euro for investigating the link between cognitive decline and cerebrovascular disease. Where Biessels focuses on clinical relevant cognitive impairment, Kessels aims to gain a better neurobiological understanding of memory. He will try and link data on memory impairment with specific brain damage as to identify brain regions involved in memory.
Cornerstone of the HiPo grant is the fact that the UMC Utrecht already maintains cohorts of elderly patients, both healthy and diabetic, also including people that have suffered a stroke. In addition, the departments that are involved have outstanding track records in research on cognitive neuroscience, cerebrovascular disease and brain imaging. Biessels and Kessels will combine information about brain functioning in diabetic patients using MRI and neuropsychological evaluations.
By and large, diabetes can be seen as an accelerator of brain ageing, it increases both diffuse atrophy and general vascular brain damage. “The concept of long-term diabetic cereberal complications is relatively new”, Biessels explains. “Following the initial discovery some fifteen years ago it took some time before the clinical relevance became clear, currently the debate is about the feasibility of prevention.”
Prevention of cognitive decline in relation to diabetes and other vascular risk factors is exactly what Biessels is after. He will use cerebral perfusion to evaluate interventions aimed at reducing vascular risk: the prescription of drugs to lower blood pressure, reduce blood clotting or lower cholesterol. By reducing vascular risk these drugs should delay the diabetes induced ageing of the brain and postpone dementia. Supposedly perfusion abormalities and subtle loss of brain volume are the pre-stage of functional impairment, which show much earlier than dementia proper. So while it takes too long to wait for dementia to develop, measuring these intermediate stages of cerebral damage may provide insight in cognitive decline. However, primary outcome should ultimately be cognitive functioning and the prevention of dementia.
“The strength of our project”, Biessels states, “lies in the in-depth analysis of cognitive decline. The combination of structural MRI, functional MRI and neuropsychological and medical assessments sheds light on the neurological mechanisms involved. An approach that fundamentally differs from large epidemiological studies.”
Methodologically one could object that diabetes associated cognitive decline is merely a side effect which will evaporate in the wake of prevention programmes aimed at reducing brain and heart infarcts. Indeed, the focus of these programmes also is on reducing high blood pressure and other factors. “However”, Biessels responds, “for all the effort that has gone in these programmes, the incidence of dementia has not decreased. Since diabetes is still on the rise, so is vascular dementia. I strongly believe a dedicated approach to vascular risk induced cognitive decline will benefit public health.”