Microtubule-associated tau protein serum level in patients with different neurodegenerative diseases

WCN 2013 No: 1814 Topic: 5 — Dementia Fluidity changes in the forebrain membranes isolated from mice bearing experimental Alzheimer's disease N. Gerasimov, A. Goloshchapov, E. Burlakova. Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, Moscow, Russia Background: Membrane structure may play a mean role in the development of dementia. Therefore, it was important to determine membrane fluidity alterations for the development of AD-like pathology. Objectives: In this work changes in fluidity of membranes isolated from the microsomal and synaptosomal fractions obtained from forebrain of mice bearing experimental Alzheimer's disease induced with olfactory bulbectomy and developed by I. Nesterova et al. [1] were studied. Materials and methods: Membrane microviscosity was measured by electron paramagnetic resonance (ESR) with 2,2,6,6-tetramethyl- 4-capryloyl-oxypiperidine-1-oxyl as lipidic and 5,6-benzo-2,2,6,6- tetramethyl-1,2,3,4-tetrahydro-γ-carboline-3-oxyl as near-proteinic probes. Rotational diffusion correlation time, characterizing mem- brane components microviscosity, was calculated from the obtained spectra of the ESR. Results and conclusions:We found out staged changes of forebrain cell membranes fluidity, accompanying AD. These alterations correlatewith the stages of «clinical» indicator changes. The main disturbance of the fluidity took place in membranes of near-protein regions. The obtained results testify the lipid peroxidation regulation system failures. Thus, the membrane structure plays an important role in the development of AD, and, taking into account these structural changes, one can better understand the course of dementia, and significantly improve the disease therapy. It was revealed that the membrane structural state was disturbed already at an early stage of experimental pathology development, modeling of AD. Hence, lipid bilayer fluidity changes can be used for early diagnostics of Alzheimer's disease. We believe that our results confirm the validity of Alzheimer s disease model based on olfactory bulbectomy proposed by N.V.Bobkova. References [1] Nesterova I, Bobkova N, Medvinskaya N, et al. Neurosci Behav Physiol 2008;38(4):349. doi:10.1016/j.jns.2013.07.1205 Abstract — WCN 2013 No: 1815 Topic: 5 — Dementia Microtubule-associated tau protein serum level in patients with different neurodegenerative diseases Y. Lekomtseva, T. Gorbach, G. Gubina-Vakulik, A. Vincent. Outpatient Clinic and Laboratory of Neuroimmunology and Biochemistry, State Institute of Neurology, Psychiatry and Narcology, NAMSU, Ukraine; Department of Biochemistry, Kharkiv National Medical University, Kharkiv, Ukraine; Department of Pathophysiology and Pathological Anatomy, Kharkiv National Medical University, Kharkiv, Ukraine; Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford University, Oxford, UK Microtubule-associated axonally-derived phosphoprotein tau is essen- tially involved into neurotoxic degenerative mechanisms: aggregation of its specific sets into filamentous inclusions is a common feature of intraneuronal and glial fibrillar lesions in numerous neurodegenerative disorders: Alzheimer's disease and Tauopathies. Tau-associated genes, proteins and Tau-phosphorylationwere also abnormal in some forms of multiple sclerosis (MS). The aim was to compare tau level in patients with temporal lobe epilepsy (TLE), relapsing remitting MS (RRMS) and amyotrophic lateral sclerosis (ALS). Method: Patients with drug-resistant long-standing TLE (n= 49; 20– 41 years), RRMS (n= 38; 27–46), ALS (n= 5; 43–58) and controls (n = 16; 25–35) were investigated. Tau was measured by immunoflu- orescent method using monoclonal anti-mouse antitau-2 antibodies also specific for phospho-Tau. Results were expressed as optical density (OD= Log10F0 / F1) units of FITC-labelled binding sites. Results: Serum tau concentration (mean± SD) under baseline condi- tions compare to controls was in TLE = 0.38 ± 0.041 vs. controls = 0.04 ± 0.002; RRMS= 1.02 ± 0.085 (P N 0.01; t = 4.69); ALS = 0.58 ± 0.06 (P N 0.01; t = 3.8). TLE that showed average tau levels had long-standing pharmaco-resistant course (mean duration ±SD: 18.5 ± 11.6) with psychiatric complications using old generation antiepileptic drugs where tau might reproduce secondary neu- rodegeneration process associated with epileptic lesion. RRMS and ALS (mean duration ± SD: 7.5 ± 2.23 and 14.2 ± 8.31, respectively) detected high tau-mediated toxicity associated in RRMS with relapses severity, and in ALS associated with cognitive decline progression as a part of tau-mediated neurodegeneration; eighteen RRMS patients formerly had brain injury (10), meningo/encephalitis virus (7) and chicken-pox (1). Conclusion: Study revealed high level of hyperphosphorylated tau in RRMS and ALS where it plays role in neurodegeneration associated with diseases severity and progression. doi:10.1016/j.jns.2013.07.1206 Abstract — WCN 2013 No: 1820 Topic: 5 — Dementia Characteristics of Parkinson's disease dementia in Southern Tunisia WCN 2013 No: 1820 Topic: 5 — Dementia Characteristics of Parkinson's disease dementia in Southern Tunisia S. Smaoui, A. Boukhris, M. Damak, E. Turki, I. Bouchhima, M.I. Miladi, I. Feki, C. Mhiri. Neurology, Habib Bourguiba Hospital, Sfax, Tunisia Objective: To determine the prevalence, characteristics and factors correlatedwith the occurrence of dementia in patients with Parkinson's disease (PD) in Southern Tunisia. Patients and methods: We recruited and examined 102 unrelated Tunisian patients with sporadic and familial PD. The mean age at onset was 64.9 years (range= 40–86) and 57.8% were men. Neuropsycho- logical evaluation was conducted and included the Unified Parkinson Abstracts / Journal of the Neurological Sciences 333 (2013) e292–e357 e324