TY - JOUR
T1 - Understanding multifactorial brain changes in type 2 diabetes
T2 - a biomarker perspective
AU - Biessels, Geert Jan
AU - Nobili, Flavio
AU - Teunissen, Charlotte E
AU - Simó, Rafael
AU - Scheltens, Philip
N1 - Funding Information:
The research of GJB is supported by Vici Grant (918·16·616) from the Netherlands Organisation for Scientific Research, and by the European Union's Horizon 2020 research and innovation programme (under grant agreement n°666881, SVDs@target, and n°847749, Recognised). The research of CET is supported by the European Commission (Marie Curie International Training Network), the Dutch Research Council (ZonMW), The Weston Brain Institute, and Alzheimer Netherlands. The research of RS is supported by a grant (SAF2016–77784) of MicEco (Spanish government), by Fundació Marató TV3 (grant 201629–10), and by the European Union's Horizon 2020 research and innovation programme (GA: 847749, recognised). We thank Tessa Timmers for providing the images for figure 1 .
Funding Information:
GJB consults for and receives research support from Boehringer Ingelheim. All financial compensation for these services is transferred to his employer, the University Medical Center Utrecht. FN has received fees from Roche, Bial, and GE Healthcare for board participation or consultation. CET has a collaboration contract with ADx Neurosciences, and did contract research or received grants from Probiodrug, AC Immune, Biogen, Esai, Toyama, Janssen Prevention Center, Boehringer, AxonNeurosciences, Fujirebio, EIP Pharma, PeopleBio, and Roche. PS has consulted for EIP Pharma, Green Valley, People Bio, Genentech, Novartis, Toyama Fuji Film, and Vivoryon. All fees are handled by and transferred to VUmc Research BV. RS has nothing to declare.
Funding Information:
The research of GJB is supported by Vici Grant (918?16?616) from the Netherlands Organisation for Scientific Research, and by the European Union's Horizon 2020 research and innovation programme (under grant agreement n?666881, SVDs@target, and n?847749, Recognised). The research of CET is supported by the European Commission (Marie Curie International Training Network), the Dutch Research Council (ZonMW), The Weston Brain Institute, and Alzheimer Netherlands. The research of RS is supported by a grant (SAF2016?77784) of MicEco (Spanish government), by Fundaci? Marat? TV3 (grant 201629?10), and by the European Union's Horizon 2020 research and innovation programme (GA: 847749, recognised). We thank Tessa Timmers for providing the images for figure 1.
Publisher Copyright:
© 2020 Elsevier Ltd
PY - 2020/8
Y1 - 2020/8
N2 - People with type 2 diabetes are at an increased risk of cognitive impairment and dementia (including Alzheimer's disease), as well as subtle forms of cognitive dysfunction. Current diabetes guidelines recommend screening for cognitive impairment in groups at high risk and providing guidance for diabetes management in patients with diabetes and cognitive impairment. Yet, no disease-modifying treatment is available and important questions remain about the mechanisms underlying diabetes-associated cognitive dysfunction. These mechanisms are likely to be multifactorial and different for subtle and more severe forms of diabetes-associated cognitive dysfunction. Over the past years, research on dementia, brain ageing, diabetes, and vascular disease has identified novel biomarkers of specific dementia aetiologies, brain parenchymal injury, and cerebral blood flow and metabolism. These markers shed light on the processes underlying diabetes-associated cognitive dysfunction, have clear applications in current research and increasingly in clinical diagnosis, and might ultimately guide targeted treatment.
AB - People with type 2 diabetes are at an increased risk of cognitive impairment and dementia (including Alzheimer's disease), as well as subtle forms of cognitive dysfunction. Current diabetes guidelines recommend screening for cognitive impairment in groups at high risk and providing guidance for diabetes management in patients with diabetes and cognitive impairment. Yet, no disease-modifying treatment is available and important questions remain about the mechanisms underlying diabetes-associated cognitive dysfunction. These mechanisms are likely to be multifactorial and different for subtle and more severe forms of diabetes-associated cognitive dysfunction. Over the past years, research on dementia, brain ageing, diabetes, and vascular disease has identified novel biomarkers of specific dementia aetiologies, brain parenchymal injury, and cerebral blood flow and metabolism. These markers shed light on the processes underlying diabetes-associated cognitive dysfunction, have clear applications in current research and increasingly in clinical diagnosis, and might ultimately guide targeted treatment.
KW - Biomarkers/metabolism
KW - Brain/pathology
KW - Cognitive Dysfunction/etiology
KW - Diabetes Mellitus, Type 2/complications
KW - Humans
UR - http://www.scopus.com/inward/record.url?scp=85085752482&partnerID=8YFLogxK
U2 - 10.1016/S1474-4422(20)30139-3
DO - 10.1016/S1474-4422(20)30139-3
M3 - Review article
C2 - 32445622
SN - 1474-4422
VL - 19
SP - 699
EP - 710
JO - Lancet Neurology
JF - Lancet Neurology
IS - 8
ER -