Clinical Neuroscience

[ASSOCIATION OF APOLIPOPROTEIN E POLYMORPHISM WITH AGE-RELATED MACULAR DEGENERATION AND ALZHEIMER’S DISEASE IN SOUTH-WESTERN HUNGARY]

KOVÁCS Á. Katalin1, PÁMER Zsuzsanna1, KOVÁCS Attila2, FEKETE Sándor2, MISETA Attila3, KOVÁCS Bálint1, KOVÁCS L. Gábor3

MARCH 20, 2007

Clinical Neuroscience - 2007;60(03-04)

[Background - Age-related macular degeneration (AMD) and Alzheimer dementia (AD) show similarities (advanced age, formation of deposits of similar content). Recently apolipoprotein E 2 (apoE 2) has been associated with AMD, while apoE4 with AD. The question of coexistence, especially with respect to the genetic background has not been studied earlier. We investigated, therefore, the occurrence of AMD in AD patients and compared their lipid profile and apoE polymorphism. Methods - 49 AMD, 32 AD and 27 control patients were examined (risk factors, visual acuity, slit lamp biomicroscopy, fundoscopy). Following measurement of triglyceride, total and HDL cholesterol levels, apoE mutation analysis was performed. Results - AMD was found in 8% of the cooperating AD patients. The prevalence of the apoE 4 isoforms in the AMD, AD and the control patients was 2%, 47% and 22%, while that of apoE 2 was 17%, 6% and 7%, respectively. The prevalence of apoE 3 isoform was 82%, 41% and 71%, respectively. Triglyceride, total and HDL cholesterol were in the reference range; however, AD patients were characterized by a lower total cholesterol value. Conclusions - The new finding of this publication is the rare occurrence of AMD among AD patients. The higher frequency of apoE 4 among the AD population, and the higher frequency of apoE 2 among AMD patients in the South-Western region of Hungary confirms the findings of other investigators.]

AFFILIATIONS

  1. Department of Ophthalmology, University of Pécs, Pécs
  2. Department of Psychiatry and Psychotherapy, University of Pécs, Pécs
  3. Department of Laboratory Medicine, University of Pécs, Pécs

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Clinical Neuroscience

[Dedication]

PALKOVITS Miklós

[Dedication 2007;60(03-04)]

Clinical Neuroscience

[Editor’s note]

RAJNA Péter

[Editor’s note 2007;60(03-04) ]

Clinical Neuroscience

[PROTECTIVE ACTION OF SNAKE VENOM NAJA NAJA OXIANA AT SPINAL CORD HEMISECTION]

ABRAHAMYAN S. Silva, MELIKSETYAN B. Irina, CHAVUSHYAN A. Vergine, ALOYAN L. Mery, SARKISSIAN S. John

[Based on data accumulated regarding the neuroprotective action of Proline-Rich-Peptide-1 (PRP-1, a fragment of neurophysin vasopressin associated hypothalamic glycoprotein consisting of 15 amino acid residues) on neurons survival and axons regeneration and taking into the account that LVV-Hemorphin-7 (LVV-H7, an opioid peptide, widely distributed in different cell types of various tissues of intact rats, including those of the nervous and immune systems) derived from the proteolitic processing of hemoglobin in response to adverse environmental and physiological conditions, possesses the anti-stressor properties, we used histochemistry, immunohistochemistry and electrophysiology to investigate the putative neuroprotective action of Central Asian Cobra Naja naja oxiana snake venom (NOX) on trauma-injured rats. ABC immunohistochemical method and histochemical method on detection of Ca2+- dependent acid phosphatase activity were used for the morpho-functional study. By recording the electrical activity of the signals from the single neurons in and below the SC injury place, NOX venom has been shown to result in the complete restoration of hypothalamic-spinal projections originated from ipsi- and contra-lateral PVN and SON to neurons of SC lumbar part. NOX prevented the scar formation, well observed two months after SC injury in the control rats, resulted in the regeneration of nerve fibers growing through the trauma region, survival of the PRP-1- and LVV-H7-immunoreactive (Ir) neurons, and increase of the PRP-1- and LVV-H7-Ir nerve fibers and astrocytes in the SC lesion region. NOX was suggested to exert the neuroprotective effect, involving the PRP-1 and LVV-H7 in the underlying mechanism of neuronal recovery.]

Clinical Neuroscience

[CENTRAL ATRIAL NATRIURETIC PEPTIDE IN DEHYDRATION]

BAHNER Udo, GEIGER Helmut, PALKOVITS Miklós, LENKEI Zsolt, LUFT C. Friedrich, HEIDLAND August

[To test the effect of dehydration on brain atrial natriuretic peptide (ANP) concentrations in areas important to salt appetite, water balance and cardiovascular regulation, we subjected rats to dehydration and rehydration and measured ANP concentration in 18 brain areas, as well as all relevant peripheral parameters. Water deprivation decreased body weight, blood pressure, urine volume, and plasma ANP, while it increased urine and plasma osmolality, angiotensin II, and vasopressin. ANP greatly increased in 17 and 18 brain areas (all cut cerebral cortex) by 24 h. Rehydration for 12 h corrected all changes evoked by dehydration, including elevated ANP levels in brain. We conclude that chronic dehydration results in increased ANP in brain areas important to salt appetite and water balance. These results support a role for ANP as a neuroregulatory substance that participates in salt and water balance.]

Clinical Neuroscience

[OXYGEN-GLUCOSE DEPRIVATION-INDUCED CHANGES IN ORGANOTYPIC CULTURES OF THE RAT HIPPOCAMPUS]

BALI Balázs, NAGY Zoltán, KOVÁCS J. Krisztina

[Introduction - (-)Deprenyl is an irreversible inhibitor of type B monoamine oxidase (MAO-B), which is now used for treatment of Parkinson’s or Alzheimer’s diseases. Evidence suggests that the neuroprotective effect of deprenyl may not be related exclusively to the inhibition of the enzyme MAO-B. Methods - To test the impact of deprenyl on ischemiainduced changes in vitro, we followed the time course of propidium iodide (PI) uptake as an indicator of neuronal cell death as well as the expression of apoptotic factors in organotypic hippocampal slice cultures exposed to oxygen- glucose deprivation (OGD) for 45 min. Results - The first signs of neuronal death were detected 2 hours after OGD and were extended to all subfields of the hippocampus by 24 hours post-injury. Presence of deprenyl (10-9 M) significantly delayed the cell death induced by the insult. Exposure of control cultures to deprenyl significantly increased the abundance of Bcl-2 and Bcl-xl mRNAs as revealed by RT-PCR. OGD resulted in an elevation of anti-apoptotic factors, while the expression of pro-apoptotic bax remained unchanged. Conclusion - These data suggest that deprenyl is neuroprotective in an in vitro model of ischemia. Although deprenyl upregulates the expression of Bcl-2 under basal conditions, its effect on anti-apoptotic factors is not significantly manifested during OGD.]

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Clinical Neuroscience

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