Browsing by Author "Potocnik, F. C. V."

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    Dementia
    (AOSIS Publishing, 2013-08-30) Potocnik, F. C. V.
    By definition, dementia is an acquired global impairment in memory, personality and intellect in an alert patient, that is sufficiently severe to interfere with social and/or occupational functioning.
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    A new model for the pathophysiology of Alzheimer's disease : aluminium toxicity is exacerbated by hydrogen peroxide and attenuated by an amyloid protein fragment and melatonin
    (Health & Medical Publishing Group, 1997) Van Rensburg, S. J.; Daniels, W. M. U.; Potocnik, F. C. V.; Van Zyl, J. M.; Taljaard, J. J. F.; Emsley, R. A.
    Objectives. Although Alzheimer's disease (AD) is the leading cause of dementia in developed countries, there is an as yet unexplained lower prevalence of the disease in parts of Africa. AD is characterised by a catastrophic loss of neurons; free radicals (oxidative toxins) have been implicated in the destruction of the cells through the process of lipid peroxidative damage of cell membranes, previously aluminium (Al) and a fragment of beta amyloid (Aβ 25-35) were shown to exacerbate free-radical damage, while melatonin reduced this effect. The aim of the present study was: (i) to investigate the conditions determining the toxicity of Al and Aβ 25-35; and (ii) to assess whether melatonin could attenuate the damage done by both aluminium and the amyloid fragment, thus suggesting a pathway for the aetiology of AD. Design. An in vitro model system was used in which free radicals were generated, causing lipid peroxidation of platelet membranes, thus simulating the disease process found in the brain. Results. 1. Al and Aβ 25-35 caused lipid peroxidation in the presence of the iron (II) ion (Fe2+), Al being more toxic than Aβ 25-35. 2. Aβ 25-35 attenuated the lipid peroxidation promoted by Al. 3. Hydrogen peroxide (H2O2) greatly exacerbated the toxicity of Al and Aβ 25-35. 4. Melatonin prevented lipid peroxidation by Al and Aβ 25-35 in the absence of H2O2, but only reduced the process when H2O2 was present. Conclusions. In the light of the results obtained from the present study, the following hypotheses are formulated. 1. In AD, excessive quantities of Al are taken up into the brain, where the Al exacerbates iron-induced lipid peroxidation in the lysosomes. 2. In response, the normal synthetic pathway of amyloid protein is altered to produce Aβ fragments which attenuate the toxicity of Al. In the process of sequestering the Al and iron, immature plaques are formed in the brain. 3. Microglia are activated, in an attempt to destroy the plaques by secreting reactive oxygen species such as H2O2. At this point in the disease process, lipid peroxidation causes a catastrophic loss of brain cells. 4. Melatonin, together with other free radical scavengers in the brain, reduces the free-radical damage caused by Al and Aβ, except in the latter stages of the disease process. Since melatonin is produced by the pineal gland only in the dark, the excess of electric light in developed countries may help explain why AD is more prevalent in these countries than in rural Africa.
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    Zinc and platelet membrane microviscosity in Alzheimer's disease. The in vivo effect of zinc on platelet membranes and cognition
    (Health & Medical Publishing Group, 1997) Potocnik, F. C. V.; Van Rensburg, S. J.; Park, C.; Taljaard, J. J. F.; Emsley, R. A.
    Objectives. To investigate the effects of oral zinc supplementation on: (i) plasma zinc concentrations; (ii) platelet membrane microviscosity in vivo; and (iii) cognitive function of Alzheimer's disease (AD) patients. Design. An open-labelled pilot study. Setting. University of Stellenbosch Medical School and Stikland Hospital. Subjects. Six volunteer AD patients. Outcome measures. Plasma zinc levels, platelet membrane microviscosity and cognition (MMSE and ADAS-cog tests). Results. Oral zinc supplementation (30 mg/day) did not increase plasma zinc levels significantly, but significantly increased platelet membrane microviscosity (P = 0.02; 6 patients). Four patients, who underwent 12 months of evaluation, showed modest cognitive improvement on psychometric testing (Mini-Mental State Examination and the cognitive portion of the Alzheimer's Disease Assessment scale scores). Conclusions. While earlier literature promoted the use of zinc in AD patients, a recent study has contradicted this and implicated zinc in the aetiology of Alzheimer's disease. On the basis of the above results, it may be premature to single out zinc as a causal agent in AD.