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Effects of lead on cholinergic SN56 neuroblastoma cells

100%
Jankowska-Kulawy A., Gul-Hinc S., Bielarczyk H., Suszkiw J. B., Pawelczyk T., Dys A., Szutowicz A.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 4
453-462
EN
Age-dependent accumulation of lead in brain has been implicated in the pathomechanisms of Alzheimer.s disease. The aim of this work was to investigate whether cholinotoxic effects of lead may result from alterations in acetyl-CoA metabolism. One day exposure of differentiated SN56 cholinergic neuroblastoma cells to 0.5 mumol/L lead or 0.01 mmol/L amyloid-beta1-42 increased fraction of nonviable cells to about 20%. Suppression of choline acetyltransferase activity occurred only in the presence of fresh amyloid-beta1-42, whereas lead was ineffective. All agents in combination caused suppression of acetyl-CoA in cytoplasm and mitochondria down to 19% and 34% of controls, respectively. Inverse correlation was observed between whole cell acetyl-CoA level and fraction of nonviable cells at different combinations of lead and other neurotoxic compounds. It indicates that lead had no primary suppressive effect on cholinergic phenotype but, at least in part, exerted cytotoxic influence on cholinergic neurons through the decrease of their acetyl-CoA.
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Molecular biology of brain aging and neurodegenerative disorders

86%
Wisniewski T., Frangione B.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
267-279
EN
A significant component of the aging process is genetically determined. Numerous theories of aging exist, many of which postulate the existence of "longevity genes". Recent advances in molecular biological and other techinques have allowed a significantly greater understanding of aging and age-related disease. This will be illustrated by four genetic and sporadic diseases: Alzheimer's disease (AD) and related disorders, transthyretin dementia, cerebral amyloid angiopathy-Icelandic type and scrapie related diseases. Alzheimer's disease (AD), the most common of this group, is the leading cause of dementia in Western countries. Recent genetic and biochemical studies have shown in involvement of at least four genes in the pathogenesis of AD. In early-onset familial AD mutations in the (beta)PP, S182 (presenilin 1) and STM2 (presenilin 2 or E5-1) genes have been found, while in the more common late-onset AD the presence of the apolipoprotein E4 isotype is a major risk factor. Genetic studies have also helped to elucidate the etiology of rarer cerebral amyloidoses such as the recently described Hungarian amyloidosis that is characterized by meningocerebrovascular amyloid deposition, with resultant dementia. This disease is linked to a mutation in the transthyretin gene. It is hoped that in the near future this increase in knowledge will allow the development of therapeutic approaches to slow the aging process.
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