Abstracts Poster sessions
TYPE 2 DIABETES IS ASSOCIATED WITH COMPACT CLOT STRUCTURE AND PROLONGED LYSIS TIME IN PATIENTS WITH CORONARY ARTERY DISEASE
S. Neergaard-Petersen1,2,3, A.M. Hvas3, S.D. Kristensen1, S.B. Larsen1, E.L. Grove1, Z. Kurdee2, P. Grant2, R.A. Ajjan2
1Department of Cardiology, Aarhus University Hospital, and Department of Clinical Medicine, Aarhus University, Denmark, 2Division of Cardiovascular and Diabetes Research, University of Leeds, United Kingdom, 3Department of Clinical Biochemistry, Aarhus University Hospital, Denmark
Background: Type 2 diabetes mellitus is associated with an increased risk of cardiovascular events and poor prognosis. Fibrin clot structure may
influence predisposition to cardiovascular events.
Aims: To investigate the influence of type 2 diabetes on fibrin clot structure in patients with coronary artery disease (CAD) treated with 75 mg aspirin daily. Underlying mechanisms to altered clot structure including
inflammation and glycaemia.
Methods: We studied fibrin clot structure and fibrinolysis in 581 CAD
patients (148 with type 2 diabetes), using turbidimetric assays and confocal and scanning electron microscopy. Inflammatory markers were evaluated by ELISA and glycaemia by HbA1c.
Results: Diabetes patients had more compact clots with increased
maximum absorbance compared with non-diabetes patients (0.36 ±0.1 vs.
0.33±0.1 au, p=0.01), associated with prolonged lysis time (804 (618; 1002) vs. 750 (624; 906) sec, p=0.03). These changes in fibrin networks were confirmed by confocal and electron microscopy. Fibrinogen levels were increased in diabetes patients (p<0.001), and using purified fibrinogen at 1 mg/mL differences in clot structure parameters were not detectable.
Inflammatory markers including CRP and C3 were increased in diabetes patients and particularly C3 correlated with clot lysis time (r=0.36, p<0.0001). HbA1c did not correlate with clot structure.
Conclusions: CAD patients with type 2 diabetes had more compact clot structure with impaired fibrinolysis compared with CAD patients without diabetes despite aspirin. This may be related to an adverse effect of type 2 diabetes on the fibrin network, coupled with increased levels of fibrinogen and inflammatory proteins.
P20.08 Eva Amalie Nielsen
ENDOTHELIN RECEPTOR BLOCKADE ABROGATE BIVENTRICULAR FIBROSIS AND RV REMODELING IN ISOLATED ELEVATED RIGHT VENTRICULAR AFTERLOAD
E.A. Nielsen1, 2, M. Sun2, V.E. Hjortdal1, A.N. Redington2, M.K. Friedberg2
1Dept. of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, and Department of Clinical Medicine, Aarhus University, 2Dept. of
Cardiology, Hospital for Sick Children, Toronto, Canada
Background: Pulmonary arterial hypertension is usually fatal due to right 174
ventricular (RV) failure. Endothelin receptor blockers are commonly used vasodilators in pulmonary arterial hypertension. Their effects on
biventricular injury and remodeling, independent of RV afterload reduction is unknown. The objective of this study was to investigate effects of
endothelin receptor blockade (ERB, Macitentan) on biventricular remodeling and function in a rabbit model of isolated RV afterload.
Methods and results: Increased RV afterload was induced by sequential pulmonary artery banding (PAB). 5 rabbits underwent PAB without ERB (positive controls); 5 received PAB + ERB; and 5 did not undergo PAB inflation (sham-operated controls (SOC)). RV and LV collagen content was increased with PAB compared to SOC and ameliorated by macitentan. LV collagen content increased in the PAB group 4.1 6.1) vs SOC 2.9 (1.7-3.7), p<0.0001 and decreased with macitentan 3.1 (0.6-5.3) vs PAB p<0.0001. RV collagen content also increased with PAB 8.3 (1.3-38.1) compared to SOC 2.9 (2.4-3.6) p<0.0001 and reduced by macitentan to 4.5 (1.6-39.5), p<0.0001. RV fibrosis signaling (connective tissue growth factor (CTGF) and endothelin-1 protein levels); extra-cellular matrix (ECM) remodeling (matrix-metalloproteinases 2 and 9), apoptosis and apoptosis-related peptides (caspases 3 and 8), were increased with PAB compared with SOC and decreased with macitentan.
Conclusion: Isolated RV afterload cause biventricular fibrosis and apoptosis, this is mediated by up-regulation of ET-1, CTGF and ECM signaling. The adverse ventricular-ventricular interactions are ameliorated by the ERB, macitentan.
P21.01 Torbjørn Halle Brøgger
DECLINING SENSITIVITY TO U46619 WITH DECREASED SIZE IN ISOLATED HUMAN SMALL VILLUS ARTERIES
T. Broegger1, A. Forman1, C. Aalkjaer2
1Department of Gynecology and Obstetrics, Skejby sygehus, Aarhus University Hospital, and Department of Clinical Medicine, Aarhus University,
2Department of Biomedicine, Aarhus University
Background: The placenta is the base for the exchange of nutrients, oxygen and waste products for the fetus. Thromboxane A2 (TxA2) is attributed a major role in control of fetal placental perfusion, which suggests potent effects in the resistance arteries. We compared the effects of the TxA2
analogue U46619, endothelin-1 and PGF2α in isolated fetal villus and maternal intramyometrial arteries of varying size.
Method: This study was approved by the Danish scientific ethical committee (j. nr 20100229). From fresh-born placentas stem villi arteries were carefully dissected, and uterine samples were harvested at caesarian section at term. Then, using wire myography, the arteries were investigated in terms of contractility and sensitivity to U46619, endothelin-1 and PGF2α in relation to their inner diameter.
Results: Fetal stem villous arteries responses to U46619 showed a positive linear correlation between pD2 and the inner diameter (r2=0.725). In contrast, responses to PGF2α and endothelin-1 showed unchanged pD2
with increasing inner diameter.
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Maternal arteries did not show any change in pD2 with different diameter when stimulated with U46619, PGF2α or endothelin-1.
Conclusion: The results suggest a selective decrease in sensitivity to TxA2
receptor stimulation with decreased vascular size in human fetal villus arteries.
P21.02 Peter Agger MYOCARDIAL REMODELLING DUE TO RIGHT VENTRICULAR DILATATION IN CONGENITAL HEART DISEASE
P. Agger1,2, C. Ilkjær1 2, C. Laustsen3, M. Smerup1, J.E. Nielsen-Kudsk4, M.
Pedersen2, V. Hjortdal1
1Research Section, Department of Cardiothoracic and Vascular Surgery (T), Aarhus University Hospital, 2Department of Clinical Medicine, Aarhus University, 3MR Center, Aarhus University Hospital, 4Dept. of Cardiology, Aarhus University Hospital
Background: Right ventricular dilatation is a well known pathological consequence of congenital heart disease mainly caused by pulmonary regurgitation. Patients with this disease have an increased risk for severe arrhythmias, heart failure and sudden death and very little is known about the aetiology of these complications and how to predict them. Today the treatment is valve substitution whenever cardiac symptoms occur, but knowledge is sparse about the optimal window for surgery. We hypothesize that morphological changes in the myocardium is the keystone in understanding this disease.
Materials and methods: The changes in myocardial architecture due to right ventricular dilatation will be investigated using diffusion tensor magnetic resonance imaging. This technique measures the spontaneous self-diffusion of water in the tissue. Using this technique in fibrous tissue, such as the myocardium, the direction of water diffusion is a measure of fibre direction. Initially, we will examine a group of piglets with induced pulmonary regurgitation and dilated right ventricle. This will be done using existing ex vivo high field 9.4T MRI protocols. Subsequently, we will attempt to establish a non-invasive in vivo setup, which can be used for clinical testing in humans.
Expected findings: We anticipate that significant changes in the right ventricular myocardial architecture will occur in the dilated right ventricle and that these changes can explain the complications in this disease.
Furthermore, we hope to be able to measure disease progression in vivo using MRI technique.
P21.03 Peter Skov Jensen
STUDIES OF THE DIAMETER RESPONSE OF SMALLER RETINAL VESSELS P.S. Jensen1, C. Aalkjaer2, T. Bek1
1Department of Ophthalmology, Aarhus University Hospital, and Department of Clinical Medicine, Aarhus University, Aarhus, Denmark,
2Department of Biomedicine, Aarhus University, Aarhus, Denmark Background: Disturbances in retinal blood flow are involved in the most
frequent causes of blindness in the Western world. The mechanisms 176
underlying the tone regulation in larger arterioles have previously been studied extensively, but evidence suggests that disturbances in the regulation of the retinal microcirculation may also play a major role in the development of vision threatening retinal diseases. However, hitherto no satisfactory in vitro model has been available for studying regulation of blood flow in the smaller retinal vessels.
Aim: To establish a method for studying the regulation of blood flow in the smaller retinal vessels in vitro.
Methods: Freshly isolated porcine retinas are mounted in a newly
developed experimental setup for studying diameter regulation of smaller retinal arterioles, followed by the study of calcium activity in the cells surrounding the vessels.
Results: Preliminary results have confirmed a different diameter regulation in larger and smaller retinal vessels, and the cellular basis for these differences will be investigated in the coming experiments.
P21.04 Martin Grann USE OF PHOTONIC FINGERPRINT AS DIAGNOSTIC TOOL AND MARKER FOR TREATMENT OF ENDOTHELIAL CELL DYSFUNCTION
M. Grann
Department of Biomedicine − Pharmacology, Aarhus University
Background: Endothelial cell dysfunction is associated with cardiovascular disease. While certain pharmacological interventions and life-style changes have been suggested to reverse endothelial cell function, early detection methods are necessary for successful implementation of such strategies. The present project is intended to aid in the development of such methods within the framework of the EU LIPHOS project in which the main concept is that of living photonics. This concept involves studying light propagated through cells to determine their spectral pattern. For distinct cell types, their morphologies as well as their conditions this light pattern has been shown to be unique and has been thus been named the photonic fingerprint (PIN).
Aim: To study the PIN and determine the living photonic patterns of healthy versus diseased cells.
Experimental methods: The PIN will be collected using a broadband light source and fiber optics from different models of cardiovascular disease. The known indicators and biomarkers of endothelial cell dysfunction will be benchmarked, using existing methods, and correlated to the changes in PIN between cell conditions and the resulting information used to create a diagnosis tool integrated with lab-on-a-chip technology.
Perspective: We aim to develop an inexpensive screening method for early detection of cardiovascular disease leading to enhanced prevention strategies.
P21.05 Simon Gabriel Comerma
ROLE OF SK3 CHANNELS IN ERECTILE FUNCTION IN MICE S. Comerma-Steffensen1, A. Kun1, E.R. Hedegaard1, C. Aalkjaer3,
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Steffensen R. Kohler2, U. Simonsen1
1Department of Biomedicine − Pulmonary and Cardiovascular Pharmacology, Aarhus University, 2Institute of Medical Biology,
Pharmacology and Physiology, University of Southern Denmark, Odense,
3Department of Biomedicine − Physiology , Aarhus University
Cardiovascular disease and erectile dysfunction are associated and share the same risk factors, and probably are linked by endothelial dysfunction.
Modulation of endothelial calcium-activated K channels has been proposed as an approach to restore endothelial function (Simonsen et al., Pharmacol. Report 2009; 61, 105-115), but the role of these channels in erectile function has not been addressed. The present study hypothesized that calcium-activated K channels with small conductance (KCa2.3 or SK3) contributes to erectile function. This was addressed in mice with either overexpression (SK3+/+) or downregulation (SK3-/-) of the SK3 channels and in wild type (WT)C57Bl/6 mice. Mean arterial pressure (MAP) as well as intracavernosal pressure (ICP) were measured in anaesthesized animals, and corpus cavernosum strips were mounted for isometric tension recording and immunoblotting was performed. MAP was decreased in SK3+/+ mice compared to WT and SK3-/- mice. Stimulation of the cavernous nerve caused frequency-dependent increases in erectile function
measured as ICP/MAP, and these responses were markedly decreased in SK3-/- mice compared to WT and SK3+/+ mice. An opener of SKCa and intermediate conductance calcium-activated K channels (IK or KCa3.1) induced concentration-dependent relaxations which were enhanced in corpus cavernosum from SK3+/+ versus SK3-/- mice, while responses to the NO donor sodium nitroprusside (SNP) were statistically unaltered. Our findings suggest that downregulation of SK3 channels blunts erectile function, and that opening of these channels may restore erectile function in disease.
P21.06 Nicolaj Christopher Hansson
MULTIDETECTOR COMPUTED TOMOGRAPHY VERSUS TRANSESOPHAGEAL ECHOCARDIOGRAPHY FOR ANNULAR SIZING IN TRANSCATHETER AORTIC VALVE REPLACEMENT
N.C. Hansson1, L. Thuesen1, V.E. Hjortdal2, J. Leipsic3, H.R. Andersen1, S.H.
Poulsen1, J.G. Webb3, E.H. Christiansen1, L.E. Rasmussen2, L.R. Krusell1, K. Terp2, K.E. Klaaborg2, M. Tang2, J.F. Lassen1, H.E. Bøtker1, B.L. Nørgaard1
1Department of Cardiology, Aarhus University Hospital, and Department of Clinical Medicine, Aarhus University, 2Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, 3Department of Medical Imaging and Division of Cardiology, St. Pauls Hospital, University of British Columbia, Vancouver, Canada
Background: Paravalvular aortic regurgitation (PAR) remains a major limitation in transcatheter aortic valve replacement (TAVR). The influence of aortic annular assessment with either multidetector computed
tomography (MDCT) or conventional transesophageal echocardiography (TEE) on the incidence of post-procedural PAR was evaluated.
Methods: In an observational study design, outcomes following TAVR with a 178
balloon expandable THV were compared in two cohorts identified
according to whether THV size selection was based on TEE (study group 1, n = 80) or MDCT (study group 2, n = 58).
Results: The two study groups were comparable with regard to baseline clinical risk score and echocardiographic characteristics. The incidence of moderate/severe PAR was lower in study group 2 than in group 1, 8.6%
versus 28.8% (p <0.01). Using receiver operating curves analysis, the difference between the THV nominal diameter and MDCT annular
diameter was predictive of moderate/severe PAR (AUC 0.84; 95% CI: 0.72-0.92). Neither age, gender, body mass index, annular eccentricity index, aortic valve calcification nor the difference between the THV diameter and the TEE annular diameter predicted post-procedural PAR. Increased THV oversizing relative to the MDCT mean annular diameter was associated with reduced severity of PAR. No difference in per-procedural complica-tions between two study groups was observed.
Conclusion: MDCT-based annular sizing in TAVR significantly reduces post-procedural PAR, and THV oversizing appears pivotal in this aspect. Further delineation of the optimal degree of THV oversizing is needed.
P21.07 Astrid Drivsholm Sloth
NO APPARENT MODIFICATION BY CARDIOVASCULAR RISK FACTORS AND COMORBIDITY ON THE EFFICACY OF REMOTE ISCHEMIC CONDITIONING BEFORE PRIMARY PERCUTANEOUS CORONARY INTERVENTION IN PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION
A.D. Sloth, M.R. Schmidt, H.E. Bøtker
Department of Cardiology, Aarhus University Hospital, and Department of Clinical Medicine, Aarhus University
Background: Remote ischemic conditioning (RIC) induces cardioprotection in patients undergoing primary percutaneous coronary intervention (pPCI) for ST-elevation myocardial infarction (STEMI). However experimental studies of myocardial infarction have demonstrated that the effect of RIC may be attenuated by comorbidity. This study evaluates the potential effect modification by cardiovascular risk factors and comorbidity on RIC in pPCI treated patients with STEMI.
Methods: The present analysis was performed on a clinical trial involving 251 patients with STEMI randomized pre-hospitally to receive pPCI with (n = 126) or without (n = 125) RIC (intermittent arm ischemia through four cycles of 5-min inflation and 5-min deflation of a blood-pressure cuff). The primary endpoint of the parent trial was myocardial salvage index estima-ted by single photon emission compuestima-ted tomography. We applied strati-fied analyses for myocardial salvage index according to the presence of cardiovascular risk factors and comorbidity to assess for effect modification.
Results: The presence of cardiovascular risk factors and comorbidity did not significantly modify the efficacy of RIC in patients with STEMI. The effect of RIC tended to be reduced in current smokers.
Conclusion: We did not identify specific cardiovascular risk factors or co-morbidity that caused significant attenuation of the efficacy of RIC. The present analysis suggests that RIC may be an effective adjunctive
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treatment in all STEMI patients regardless of cardiovascular risk factors and comorbidity. Our findings need confirmation in large-scale randomized clinical trials.
P21.08 Nikolai Hoffmann-Petersen
A COMPARISON OF OFFICE BLOOD PRESSURE, TELEMEDICAL HOME BLOOD PRESSURE AND AMBULATORY BLOOD PRESSURE MONITORING N. Hoffmann-Petersen, J.N. Bech, E.B. Pedersen
Departments of Medical Research and Medicine, Holstebro Hospital Background: Telemonitoring of home blood pressure is a new advance in
blood pressure monitoring (HBPM). The aim of this study was to compare the accuracy of office blood pressure and telemedical home blood pressure with 24-h ambulatory blood pressure (AMPM).
Methods: 102 patients were consecutively recruited from a Renal Out-patient Clinic. Office blood pressure was measured three times with HBPM equipment. Next patients used HBPM with telemonitoring three times daily for four consecutive days and finally ABPM on the following day.
Results: There was a significant difference between OBPM and ABPM (24-h and daytime) and between HBPM and daytime ABPM; HBPM was lower (-4.1 mmHg/-1.6 mmHg) than daytime ABPM (p<0.05). The strongest correlations were seen between all HBPM readings day 2-4 and ABPM (24-h and daytime). T(24-here was no significant difference between HBPM and 24-h ABPM.
Conclusion: The telemedical HBPM reflected more accurately 24-h ABPM than office readings.
P21.09 Lisbeth Bonde EXTRACELLULAR ACIDIFICATION INHIBITS NA+,HCO3- -COTRANSPORT ACTIVITY
L. Bonde, C. Aalkjaer, E. Boedtkjer
Department of Biomedicine, Aarhus University
Background: In the vascular smooth muscle cells of resistance arteries, the net acid extrusion is primarily mediated by the Na+/H+-exchanger NHE1 and the electroneutral Na+,HCO3- -cotransporter NBCn1. Both transporters are activated upon intracellular acidification and contribute to a rapid recovery of intracellular pH (pHi). Extracellular acidification has been demonstrated to inhibit Na+/H+ -exchange but the effect of extracellular pH (pHo) on NBCn1 activity has not yet been clarified.
Aim: The present study aimed to investigate the effect of pHo on NBCn1.
Method: We used BCECF-based fluorescence microscopy to study pHi dy-namics. Mesenteric arteries were isolated from male NMRI mice and kept in physiological saline solution. After intracellular acidification induced by addition of 20 mM NH4Cl and subsequent washout, the pHi recovery was measured in the presence and absence of CO2/HCO3- and 1 mM amiloride at pHo 7.4, 7.1 and 6.8. Groups were compared by one-way ANOVA.
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Results: NHE1 transport rates in the pHi range 6.7-6.8 gradually decreased when pHo was reduced. The Na+/H+-exchange activity decreased by 26 ± 7% (means ± SEM, p<0.05, n=6) when pHo was changed from 7.4 to 7.1, and by 66 ± 14% (p<0.01, n=6) when pHo was reduced to 6.8. NBCn1 activity in the pHi range 6.7-6.8 was also significantly inhibited (59 ± 10%;
p<0.01, n=6) by a pHo decrease from 7.4 to 6.8. Yet, the transporter was resistant to moderate changes in pHo as no change in Na+,HCO3 -cotransport activity (9 ± 11%; p=0.43, n=6) was seen when pHo was changed from 7.4 to 7.1.
P22.01 Jacob Reinholdt Jensen
INITIATION OF CANCER INVESTIGATIONS IN GENERAL PRACTICE J.R. Jensen1, P. Vedsted1, H. Møller2, J.L. Thomsen3, M.B. Christensen4
1Research Centre for Cancer Diagnosis in Primary Care (CaP), Department of Public Health, Aarhus University, 2Cancer Epidemiology and Population Health, King's College, London, 3Dansk Almenmedicinsk Kvalitetsenhed (DAK-e), 4Research Unit for General Practice, Aarhus
Background: Close to 90% of all cancers are diagnosed because the patient presents symptoms and signs. Of these patients, 85% initiate the diagnostic pathway in general practice. Therefore, the initiation of a diagnostic pathway in general practice becomes extremely important. On average, a general practitioner (GP) is involved in 7500 consultations each year, and in the diagnostic process of 8-10 incident cancers.
One half of cancer patients consult their GP with either general symptoms, which are not indicative of cancer, or vague and non-specific symptoms.
The other half present with what the GP assess as alarm symptoms. Three months prior to diagnosis, patients who are later diagnosed with cancer have twice as many GP consultations than a comparable reference population. Thus the complex diagnostic process in general practice requires the GP to react on very different and vague symptoms to ensure early cancer diagnosis. To enable earlier cancer diagnosis, we need much more knowledge and a better understanding of the initiation of cancer-specific tests and investigations in general practice.
Aim: To investigate how, how often and on which background investigation for suspected cancer is initiated in general practice.
Methods: Participating Danish GPs will fill in an electronic questionnaire after random consultations. A total of 70,000 consultations will be included.
Perspectives: The results will show how often and why GPs suspect cancer, how they perform the initial investigations and whether this process can be supported and optimised. This insight is crucial in order to improve the diagnostic pathway.
P22.02 Niels Peter Andersen
NON-INVASIVE REDUCTION IN NERVE CONDUCTIVITY IN CLOSE RELATION TO FLOW, USING MRI-GUIDED HIGH INTENSITY FOCUSED ULTRASOUND (HIFU)
N.P Andersen1, Dam1, Madsen2, K. Beedholm2, P. Teglberg Madsen2, S.
Hansen1, P. Hokland3, Fjord Petersen1, S. Buus4, B. Svedsen4, M. Pedersen1
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1Institute of Clinical Medicine, 2Department of Zoophysiology, 3Department of Radiotherapy, 4Department of Nephrology, Aarhus University Hopital, Denmark
Background: Resistant hypertension, a leading cause of death worldwide, is caused by hyperactivity of the sympathetic nerves in the walls of the renal artery. When orally administrated, antihypertensive drugs have no effect, and patients with resistant hypertension are subjected to renal denervation, using an invasive catheter-based (radiofrequency) ablation technique. We hypothesize that a non-invasive method of renal denervation could be performed using MRI-guided High Intensity Focused Ultrasound (HIFU). To address this, our first step was to demonstrate the usefulness of MRI-guided HIFU for nerve damage in close relation to major vessel flow.
Materials and methods: Danish landrace pigs (30 kg, n=6) were positioned in a Philips Sonalleve HIFU system with the neck area facing down towards a multielement HIFU transducer. HIFU treatments were made on one vagus nerve while the contra lateral side served as control. Neurophysiological conductivity tests of the nerves were after the Ultrasound treatments carried out, with a stepwise increase in voltage (0.2, 2.0 and 20 V).
Results: We were able to successfully target the vagus nerve with MRI-guided HIFU. Neurophysiological investigations showed a significant reduction in nerve conductivity in the heat-treated vagus nerve in comparison to the non-sonicated side.
Conclusion: This study demonstrated that we were capable of delivering enough energy using MRI-guided HIFU to reduce function significantly in nerves (vagus) adjacent to the major vessels with large flow, which are suspected to reduce the effect of sonication due to the thermodynamic cooling of flowing blood. These encouraging results motivate our next step:
renal denervation.
P22.03 Rasmus Hansen Olesen
BLOOD BRAIN GLUCOSE TRANSPORT IN RELATION TO INCREASING BMI EXPRESSION OF GLUT1 AND GLUT3 IN THE PREFRONTAL CORTEX
R.H. Olesen1, M.G. Jensen1, J.E. Kleinman2, T.M. Hyde2, J. Rungby1, A. Larsen1
1Department of Biomedicine - Pharmacology, Aarhus University, 2Lieber Institute for Brain Development, Baltimore, USA
Background and aims: Excess body weight is a major health problem, leading to increased mortality and morbidity. There seems to be a relationship between elevated BMI and reduced cognitive performance.
Recent research links obesity to increased risk of Alzheimer's Disease (AD).
Glucose enters the brain by facilitated diffusion across the Blood Brain Barrier (BBB). Under normal conditions, glucose transport across the BBB does not affect the cerebral glucose metabolism but under pathophysio-logical conditions, the transport of glucose can be rate limiting. In AD, the cerebral metabolic rate of glucose is decreased in the most affected regions. We hypothesize that chronic metabolic changes induce alterations in the glucose transport over the BBB and that this will be reflected when comparing obese and normal weight individuals.
Materials and methods: The BrainCloud contains gene expression data on 182