Poster Presentations P1 P1-126
A CASE PRESENTING WITH DIALYSIS DEMENTIA
Gu¨lden Akdal, Go¨rsev Gu¨lmen Yener, Barıs¸ Baklan, Erdem Yaka. Dokuz Eylul University Faculty of Medicine Department of Neurology, I˙zmir, Turkey. Contact e-mail:
[email protected] Background: Dialysis dementia may occur in the course of dialysis. Objective: To emphasize the relation of progressive dementia and dialysis. Method: A 67 year old man who was taking dialysis was consulted with the presentation of rapid progressive memory disturbance and speech problem.We performed blood, urine screening tests, neuroimaging and EEG in order to find out the cause of dementia. Results: History revealed that he was having dialysis for the last four years and rapid progressive memory problems for the last six months. Neurological examination (NE) showed non-cooperativeness, disorientation, dysarthria, bilateral positive Babinski sign, normal muscle bulk and strength. Patient could not walk due to possible apraxia. Computed tomography displayed diffuse atrophic changes and a left lacunar infarction in the posterior limb of internal capsule. EEG revealed bilateral left dominant frontotemporal slow wave complexes. Neuropsychological tests could not be given because of non-cooperativeness of patient. Diagnosis of dialysis dementia was made by history, clinical findings and EEG features. A few months after the diagnosis patient passed away. Conclusion: Prevalance of dialysis dementia has been estimated at around 0.6% to 1.0% nowadays. If it is diagnosed earlier, desferrioxamine infusions which is the mainstay of treatment can be started earlier.
P1-127
DISTINGUISHING NEURODEGENERATIVE DISORDERS WITH TAU PATHOLOGY USING MRNA EXPRESSION MICROARRAYS
Iraad F. Bronner1,2, Zoltan Bochdanovits1,2, Patrizia Rizzu1,2, Wouter Kamphorst3, Rivka Ravid4, John C. van Swieten5, Peter Heutink1,2. 1VU University Medical Center, Department of Human Genetics, Section Medical Genomics, Amsterdam, The Netherlands; 2 Center for Neurogenomics and Cognitive Research, VU University Medical Center and VU University, Amsterdam, The Netherlands; 3VU University Medical Center, Department of Pathology, Amsterdam, The Netherlands; 4The Netherlands Brain Bank, Amsterdam, The Netherlands; 5Erasmus Medical Center, Department of Neurology, Rotterdam, The Netherlands. Contact e-mail:
[email protected] Background: Despite intensive research, the etiology of Alzheimer’s disease (AD), Pick’s disease (PiD), Progressive Supranuclear Palsy (PSP) and Frontotemporal dementia (FTD) is still largely unknown. Due to the overlap between these diseases clinical diagnosis of these patients is difficult. Even on post-mortem material classification of disease type is labour intensive and complex. Objective: Microarrays can provide insight in the complexity and relationships between diseases and normal aging, as they provide data of the simultaneous activity of multiple genes and cellular pathways. This makes microarrays an ideal platform for disease classification. Our objective was to investigate whether microarrays can be used for disease classification. Methods: We analysed snap frozen post-mortem tissue from the medial temporal lobe of pathology confirmed patients with four different tauopathies AD, PSP, PiD, FTD and control subjects for gene expression. To exclude as much non-disease-related variation all patients were age, gender, APOE-⑀ and MAPT (tau) haplotype matched. Results and Conclusions: Using several rounds of analysis we identified a set of 166 genes that can discriminate all patient groups from controls. Furthermore PSP and AD and FTD/PiD also clustered into separate clusters. These findings are a first step towards the development of an accurate microarray-based classification test.
P1-128
S133 NON-INVASIVE EARLY DETECTION OF BETAAMYLOID MOLECULAR PATHOLOGY BY QUASI-ELASTIC LIGHT SCATTERING IN VIVO
Lee E. Goldstein1, Robert Moir2, Suqian Lu1, Ling Fu1, Oliver Chadwick2, Ernest Arnett3, Maria Ericsson4, William Klunk5, Chester Mathis5, Leo T. Chylack, Jr.1, John Clark3, Rudolph Tanzi2, Juliet A. Moncaster1. 1Brigham & Women’s Hospital/Harvard Medical School, Boston, MA, USA; 2Massachusetts General Hospital/Harvard Medical School, Charlestown, MA, USA; 3University of Washington School of Medicine, Seattle, WA, USA; 4Harvard Medical School EM Facility, Boston, MA, USA; 5University of Pittsburgh Medical School, Pittsburgh, PA, USA. Contact e-mail:
[email protected] Background: Sensitive, specific, objective diagnostic tests for Alzheimer’s disease (AD) are urgently needed for efficient drug development and effective clinical use of emerging therapies. Enabling AD diagnostic technology will accelerate preclinical drug discovery, streamline clinical testing, and facilitate therapeutic intervention. Patient care will be enhanced by an objective means to assess AD risk, establish early diagnosis/prognosis, initiate therapeutic intervention, track disease progression, and monitor treatment response. We previously reported discovery of beta-amyloid peptides, AD-associated amyloid pathology, and unusual co-localizing equatorial supranuclear cataracts in the ocular lenses of patients with AD but not in those without the disorder [Lancet, 2003]. We recently discovered and characterized similar beta-amyloid lens pathology in patients with Down syndrome and in Tg2576 transgenic mice. These findings provide the first evidence of AD-associated beta-amyloid pathology outside the brain and support a direct molecular link between AD-associated pathology in brain and lens. Objectives: To develop and test novel laser technology for early quantitative detection/monitoring of ADassociated amyloid lens pathology in vivo. Methods: Non-invasive infrared quasi-elastic light scattering (QLS), stereophotomicroscopy, quantitative western blot, ELISA. Results: We developed in vivo QLS technology to quantitatively assess amyloid-mediated lens protein aggregation within discrete lens subregions. The instrument is easy to use, reliable, and extremely sensitive. We tested this non-invasive technology in non-anesthetized Tg2576 and agematched WT control mice. Non-invasive lens QLS measurements (right-angle scattering intensity, It90) completely differentiated Tg2576 vs age-matched WT controls at 10 months of age, when cerebral and lenticular amyloid pathology are minimal. Preclinical testing using systemic or topical administration of a lipophilic amyloid-binding fluorescent ligand demonstrates anatomically localized amyloid-associated lenticular fluorescence in vivo. Conclusions: Non-invasive quantitative laser technologies hold promise for early diagnostic assessment of AD-associated pathology in vivo. Support: NIA (AG024792, LG), NIGMS (GM075986); Alzheimer’s Association, Massachusetts Lion’s Eye Research Fund, MA Alzheimer’s Disease Research Center, Brigham & Women’s Hosp, anonymous foundations. P1-129
LACK OF IDENTIFICATION OF COGNITIVE IMPAIRMENT IN THE ELDERLY BY THE GENERAL PRACTITIONER IN BRAZIL PRELIMINARY RESULTS
Alessandro F. Jacinto. University of Sa˜o Paulo, Sa˜o Paulo, Brazil. Contact e-mail:
[email protected] Objectives: To verify if elderly patients have their cognitive impairment diagnosed by general practitioners. Methods: A sample of elderly patients who have been followed by general practitioners were randomly selected and invited by telephone to participate in a clinical research, and submitted to a cognitive and functional evaluation by a geriatrician. MMSE and/or IQCODE scores were chosen to classify these individuals into suspects of cognitive impairment or not. Those who were classified as suspects underwent neuropsychological testing consisting of a group of tests named Mattis Dementia Rating Scale. The general practitioners’ files of patients with cognitive impairment and of a sample of patients without cognitive impairment were checked out. Results: 152 patients (78 women), mean age 72.0 (5.3) years and
