Seminar : MIG Seminar by Dr Geert Jan Biessels
The Metabolic Interest Group is pleased to present an upcoming seminar:
Diabetes, cognitive dysfunction and dementia,
implications for daily care and research
19 February 2009
11:30 - 12:30pm, Lunch to follow
SBIC Seminar Room, Biopolis Helios Level 2
(Entrance via SBIC Level 1)
All are welcome!
Please send your details to
email@example.com for registration
Registration closes on 16 February 2009.
Geert Jan Biessels,
Department of Neurology, University Medical Centre Utrecht
Geert Jan Biessels is a neurologist at the University Medical Centre Utrecht, the Netherlands. His research, at the Department of Neurology of the Rudolf Magnus Institute for Neuroscience, focuses on the effects of diabetes on cognitive functioning, and on other vascular causes for cognitive decline and dementia. His PhD studies, completed in 1997, involved a series of experiments on cognition and synaptic plasticity in experimental diabetes in rats. He is one of the founders and project leader of the Utrecht Diabetic Encephalopathy Study Group. This study group aims to elucidate the nature, severity and pathophysiology of accelerated cognitive decline in patients with diabetes through detailed neuropsychological assessment, in combination with brain imaging and examination of metabolic and vascular risk factors. He is (co)author of a substantial number of papers on peripheral and central neurological complications of diabetes, and is board member of Neurodiab, the Diabetic Neuropathy Study Group of the European Association for the Study of Diabetes.
It is now well accepted that diabetes mellitus is associated with cognitive dysfunction and abnormalities on brain imaging. Recent studies provide new leads on underlying mechanisms as well as insight into the nature and severity of these cerebral complications. This helps to explain why some diabetic patients show clinically significant cognitive morbidity, whereas a large proportion of patients is apparently unaffected. It appears that clinically relevant diabetes-related cognitive decrements mainly occur in two ‘critical periods' in life: the period of brain development in childhood and the period when the brain is undergoing neurodegenerative changes associated with aging. In children this involves impairment of cognitive development, to a level that may have an impact on school achievement. In older patients with type 2 diabetes this involves a 1.5 to 2 times increased risk of dementia (Alzheimer's disease, as well as vascular dementia) and an increased risk of cognitive disturbances short of dementia (e.g. Mild Cognitive Impairment (MCI)). Evidently, risk factors and mechanisms for cognitive decrements also differ across age groups and diabetes types.
Over the past few years there has been important progress in mechanistic studies. While such studies initially focused on vascular disturbances and adverse effects of high glucose levels on the brain it is now becoming clear that disturbances in insulin signaling are a potentially important lead in the pathogenesis, particularly with regard to the observed link between type 2 diabetes and Alzheimer's disease. Alterations in insulin signaling have been shown to affect cerebral amyloid and tau metabolism and affect synaptic plasticity in the brain. The challenge for the coming decades will be to dissect out the mechanisms that drive the association between diabetes and cognitive decrements in different age groups, in relation to diabetes type. Insight into these mechanisms will help to prevent clinically relevant cognitive decrements in patient groups that are at particular risk for such decrements.
Co-organized by the A*STAR Metabolic Interest Group and the NUHS Dementia Research Programme.
Tue, 10 Feb 2009
Seminar : Seminar by Dr Henry Boom
Infection and Immunity Seminar
Evasion of T cell immunity by M. tuberculosis: a role for mycobacterial lipoproteins, glycolipids and TLRs.
By Dr Henry Boom
Tuberculosis Research Unit (TBRU) and Division of Infectious DiseasesCase Western Reserve University School of Medicine
10 February 2009, 10:00 - 11:00am
30 Biopolis Street, S138671
Level 4, Breakthrough Threaterette
All are welcome and no pre-registration is required.
Dr Henry Boom obtained his MD from University of Rochester in 1979. In 1995, he became an Associate Professor and was later appointed the Vice Chair for Research and Professor in the Department of Medicine, and the Director of Tuberculosis Research Unit (TBRU), Case Western Reserve University. He is the winner of the Individual National Research Service Award by NIH from 1986 - 1988 and Excellence in Research Award (AFCR) 1990. Dr Henry Boom's main research interest focuses on the cellular immune response to intra-cellular pathogens such as Mycobacterium tuberculosis.
Mycobacterium tuberculosis (MTB) is readily transmitted by inhalation of aerosolized mycobacteria. As T cell immunity develops in the lung, growth of MTB is controlled. However despite robust activation of host immunity, MTB evades innate and adaptive immune responses to survive and persist in order to reactivate when T cell immunity wanes due to aging, malnutrition, HIV, etc. My lab. is focused on defining molecular mechanisms used by MTB to evade CD4+ T cell responses by combining biochemical and molecular approaches to the purification of mycobacterial molecules with assays of human and murine CD4+ T cell function in vitro and in vivo. We are currently working on four distinct mechanisms. We have found that prolonged TLR-2 stimulation by mycobacterial lipoproteins inhibits MHC-II antigen processing by macrophages for CD4+ T cells. Furthermore MTB phosphotidyl-inositol mannoside (PIM) can interact with VLA-5 (Valpha5beta1) on CD4+ T cells, inducing adhesion to fibronectin and thus modulation of T cell migration in granulomas. The MTB cell wall also contains additional molecules that directly affect TCR signaling and CD4+ T cell co-stimulation. Thus the MTB cell wall is a particularly rich source of molecules that directly and indirectly affect CD4+ T cell recognition of MTB, and thereby determine the balance between the host's ability to optimally activate T cells, and MTB's ability to evade T cell recognition.
This seminar is organized by the Infection and Immunity Program, SICS.