Modulation of vitamin E processing in brain by apolipoprotein E

Modulation of vitamin E processing in brain by apolipoprotein E

280 Abstracts / Journal of the Neurological Sciences 283 (2009) 240–320 White Matter Lesions Semiquantitive Rating Scale, taking into consideration ...

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280

Abstracts / Journal of the Neurological Sciences 283 (2009) 240–320

White Matter Lesions Semiquantitive Rating Scale, taking into consideration the amount, size and distribution of WML. Results: WML of the brain were seen in all patients with AD and MCI on T2 and FLAIR sequences. The positive correlation between the patients' age and the amount and size of WML, in the subcortical (T2: p < 0.05, r = 0.30) and in the periventricular region (T2: p < 0.005, r = 0.39; FLAIR: p < 0.05, r = 0.29) has been shown on both sequences. There was no correlation between the size or distribution of lesions and either hypertension or homocysteine blood level. The analysis showed also that in both sequences, the amount of lesions in the periventricular region increased with the progression of the disease (T2: p = 0.038; FLAIR: p = 0.02). Conclusions: The significant factor correlating with the location of WML in patients with MCI and AD is the age of a patient. The amount and size of WML in the periventricular region of the brain depends on the severity of dementia. Hypertension and homocysteine blood level has no influence on the presence of described lesions. doi:10.1016/j.jns.2009.02.154

White matter hyperintensities as a microvascular mechanism mediating memory impairment in elderly persons with type 2 diabetes J.A. Luchsingera,d,e,f, A. Riveroa, W. Palmasa, L. Fieldg, S. Sheaa,d, R. Mayeuxb,c,d,e,f Department of Medicine, Columbia University Medical Center, New York, NY, USA b Department of Neurology, Columbia University Medical Center, New York, NY, USA c Department of Psychiatry, Columbia University Medical Center, New York, NY, USA d Department of Epidemiology, Joseph P. Mailman School of Public Health, Columbia University, New York, NY, USA e Taub Institute For Research On Alzheimer's Disease and The Aging Brain, Columbia University, New York, NY, USA f Gertrude H. Sergievsky Center, Columbia University, New York, NY, USA g School of Nursing, Columbia University, New York, NY, New York, NY, USA

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Background: memory impairment may be a microvascular complication of type 2 diabetes (T2D). We explored the relation between white matter hyperintensities (WMH) and memory among persons with T2D. Methods: 77 elderly persons with T2D and without history of clinical stroke aged 71.7± 6.6 years underwent structural brain MRI; 71% were women, 73% Caribbean-Hispanic, 20% African American, and 7% Non-Hispanic-White. WMH volume was adjusted for cranial size and required logarithmic transformation. Memory was assessed with Buschke’s Selective Reminding Test (SRT). Covariates included demographics and HbA1c, systolic blood pressure, low density lipoprotein, and urine microalbumin/creatinine ratio. Results: The strongest correlates (Pearson correlation) of WMH were age (r = 0.34; p = 0.003), HbA1C (r = 0.33; p = 0.004), and microalbuminuria (r = 0.41; p = 0.0004). WMH was inversely related to SRT total recall using linear regression after adjustment for age, sex, and education (− 4.1; p = 0.0003). Examination of total recall of the SRT by quartiles of WMH using ANACOVA revealed a dose response association. The mean total word recall for each quartile of WMH adjusted for age, sex, and education, from first to last were 38.5, 34.8, 31.9, 31.1 (p for trend = 0.004). Adjusting for microalbuminuria and HbA1c appreciably attenuated this association (p for trend = 0.36). Conclusion: WMH and memory are strongly related in persons with T2D. This association was mediated by glucose control and microvascular disease consistent with the hypothesis that memory impairment is in part a microvascular complication of T2D.

tritium-labeled alpha tocopherol was injected into the lateral cerebral ventricle and its uptake by different regions of the brain of apoE deficient and wild type mice was determined. Eleven week-old apoE deficient and wild type mice were fed normal rodent chow. Intravenously injected alpha tocopherol was poorly incorporated by the brain; hence ventricular injection was employed When labeled cholesterol was injected simultaneously it was incorporated in a pattern that was very similar to that of tocopherol. Therefore, cholesterol uptake was used as an internal standard to account for experimental variability of injection and other factors. As expected, regions close to the site of injection and those with high surface areas in contact with spinal fluid showed higher uptake of radioactive alpha tocopherol (e.g., hippocampus and striatum more than cerebral cortex). Most areas of apoE deficient brains showed a decrease in uptake of radioactive tocopherol per gram wet weight. Alterations in the clearance and transport of tocopherol (possibly mediated by apoE) might be the reason for this decline in uptake. Nearly all of the injected alpha tocopherol was unchanged in the brains of both apoE deficient and wild type animals suggesting low turnover rate. Overall, the current data reinforce the hypothesis that apoE is a key protein involved with the transport and/or retention of alpha tocopherol in brain. Supported by Medical Research Funds from the Dept. of Veterans Affairs, Washington DC. doi:10.1016/j.jns.2009.02.156

Soluble amyloid-B and secretory phospolipase A2 Biochemical markers for early diagnosis of Alzheimer disease B.O. Pasaribua, A. Wijayaa, A. Hamidb Faculty of Medicine, Hasanuddin University, Makassar, Indonesia b Faculty of Medicine, Indonesia University, Jakarta, Indonesia

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Background and aims: Dementia is related to aging, and with the increasing numbers of elderly people in the population, the number of patients with dementia is growing rapidly. The major cause of dementia is Alzheimer's disease (AD). Biochemical process and pathological alterations in the Alzheimer disease brain result from cellular processes such as amyloid precursor protein (APP) and amyloid b-protein metabolism, tau phosporylation, oxidative stress, inflammation, and lipid dysregulation. Currently there are no simple test or biochemical markers that could detect all early AD cases, and the definite diagnosis of AD is based on histopathological evidence obtained from autopsy. With the development of new therapeutic strategies, and the concept of mild cognitive impairment (MCI) as an early stage of AD, there is an increasing need for an early and accurate biomarker for AD diagnosis. Methods: The design of this study is case control analyses in 17 AD patients, 13 MCI patients and 8 control subjects in Pasar Minggu Polyclinic — Jakarta and Usada Mulia Old Age Home — Jakarta, grouped based on Mini Mental State Examination (MMSE) and Clinical Dementia Rating (CDR) test. Diagnostic criteriation of heart failure was established with MMSE and CDR score. Amyloid-b and sPLA2 were measured with Enzyme-Linked Immunosorbent Assay (ELISA). Result: Patient's age was 65.04±7.2 years. There is a significant differences between AD patients and control and between MCI patients and control (amyloid-b : r=0.441⁎⁎p =0.01 and sPLA2 : r =0.347 ⁎⁎p =0.007). Conclusion: This study suggested that amyloid-b and sPLA2 has been implicated in the progression of AD and can be support the diagnosis of AD from early stages of the disease (MCI). doi:10.1016/j.jns.2009.02.157

doi:10.1016/j.jns.2009.02.155

Modulation of vitamin E processing in brain by apolipoprotein E G.T. Vatasserya,b, W.E.D. Smitha, H.T. Quacha V. A. Medical Center, Minneapolis, MN, USA b University of Minnesota, Minneapolis, MN, USA a

Abnormal function of apolipoprotein E (apoE) has been implicated in the incidence of some neurological disorders including dementia. We have recently observed that brain alpha tocopherol (vitamin E) levels are altered in apoE deficiency (Vatassery et al. J. Neurosci. Res. 84: 1335–72, 2006). In this study,

Communication between endoplamic reticulum and mitochondria in the neuronal death induced by amyloid-beta peptide E. Ferreiro, R. Costa, R. Resende, S. Marques, S. Cardoso, C.R. Oliveira, C. Pereira Center For Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal Alzheimer's disease (AD) is a progressive and fatal disorder of the central nervous system with relevant social impact, characterized by progressive memory loss and deterioration of cognitive functions. An increasing body of evidence