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BACKGROUND AND AIMS: Excess of zinc ions and intermittent hypoxia both cause neurodegeneration by disruption in energy metabolism and oxidative stress, resulting in diminished pyruvate dehydrogenase complex (PDHC) and aconitase activity and consequent shortages in acetyl-CoA. This deficiency may be particularly dangerous for cholinergic neurons as they consume acetyl-CoA in additional pathway of acetylcholine...
BACKGROUND AND AIMS: The aim of this work was to find relationships between Zn accumulation and integrity of cholinergic and astroglial cells. METHODS: Exposition of cAMP/RA-differentiated (DC) and nondifferentiated (NC) cells cholinergic SN56 neuroblastoma and astroglial C6 cells to Zn yielded its concentration dependent accumulation. The level of Zn was measured by fluorimetric method with TSQ....
BACKGROUND AND AIMS: Cholinergic neurons produce acetylCoA, which is subsequently used as a fuel for energy production. Furthermore, exclusively those neurons produce acetylcholine from acetyl-CoA. As a results, extra utilization pathway may induce acetyl-CoA shortages and consequently impairment of brain energy metabolism. Disturbances in Ca-signaling could play regulatory role in neurons susceptibility...
BACKGROUND AND AIMS: Inhibition of brain energy metabolism, accompanied by inflammatory activation of microglial cells is a characteristic feature of several neurodegenerative brain diseases, including Alzheimer’s, aluminum or vascular encephalopathies. Microglial inflammatory response to neurotoxic signals may contribute to neuronal degeneration through excessive production of nitric oxide (NO) and...
Acetyl-CoA synthesized from glucose-derived pyruvate by pyruvate dehydrogenase complex (PDHC) is a main substrate, for mitochondrial energy production and cytoplasmic synthetic pathways in all types of brain cells. Activities of mitochondrial PDHC, and several enzymes of acetyl-CoA metabolism, and ZnT1 transporter level in cholinergic septal SN56 cells were from 2 to 8 times higher than those in microglial...
Microglial cells, through the proinflammatory mediators play an important role in host defense and tissue repair in CNS. They contribute to pathomechanisms of Alzheimer’s and other neurodegenerative diseases. The aim of this work was to investigate modifying effects of non-activated migroglia on cholinergic neuronal SN56 cells subjected to common neuroprotective and/or neurotoxic signals. Chronic...
Cholinergic neurons of brain septum were found to be highly susceptible to neurodegenerative conditions. The sources of this particular sensitivity remain unclear. There is suggestion that their low resistance to cytotoxic conditions might be due to comprehensive consumption of acetyl-CoA. In cholinergic neurons the acetyl-CoA, except of intramitochondrial utilization for energy and NAA synthesis,...
Inhibition of pyruvate (PDHC) and ketoglutarate (KDHC) dehydrogenase complexes induced by thiamine pyrophosphate deficits is known to cause disturbances of cholinergic transmission in the brain, yielding clinical symptoms of cognitive and motor deficits. However, particular alterations in distribution of acetyl-CoA, in the glial cells of thiamine pyrophosphate-deficient brain remain unknown. Therefore,...
Zinc excess in the synaptic cleft may be one of pathologic signals triggering chronic neurodegenerative events. The aim of this work was to find relationships between Zn accumulation and integrity of cholinergic and astroglial cells. Exposition of cAMP/RA-differentiated (DC) and nondifferentiated cells (NC) cholinergic SN56 neuroblastoma and astroglial C6 cells to Zn yielded its concentration dependent...
Inhibition of pyruvate (PDHC) and ketoglutarate (KDHC) dehydrogenase complexes induced by thiamine pyrophosphate deficits is known cause of disturbances of cholinergic transmission in the brain, yielding clinical symptoms of cognitive, vegetative and motor deficits. However, particular alterations in distribution of key acetylcholine precursor, acetyl-CoA, in the cholinergic neuron compartment of...
Preferential loss of septal cholinergic neurons is a main cause of cognitive deficits in various encephalopathies. Zinc excess is one of multiple pathologic signals contributing to mechanisms of Alzheimer’s and other neurodegenerative diseases. We suggest that zinc may be involved in early excitotoxic phase of neuronal injury. In homogenates of SN56 cholinergic neuroblastoma cells, Zn caused instant...
Inhibition of brain energy metabolism in demented subjects correlates with impairment their cognitive functions and loss of cholinergic neuron markers found in post mortem studies. However, mechanisms of preferential loss of brain cholinergic neurons in Alzheimer’s disease and other encephalopathies, remain unknown. We demonstrate that neuronal acetyl-CoA metabolism may be a primary target for neurodegenerative...
Cholinergic neurons like the other ones may synthesize N-acetylL-aspartate (NAA), which serves as a source for acetyl units for lipid synthesis in oligodendroglial cells. Pyruvate-derived acetylCoA is a substrate for NAA synthesis in aspartoacylase reaction in the mitochondrial and cytoplasmic compartments of neuronal cells. Highly differentiated cholinergic neurons were found to be more susceptible...
Neurodegenerative lesions in cholinergic encephalopathies include an excessive activation of microglia, which may aggravate this process. Infl amatory cytokines were reported to affect viability of cultured cholinergic cells, through the infl uence on their acetyl-CoA metabolism. The aim of this work was to investigate whether phenotypic modifi cations of N9 microglia by common neuron-differentiating...
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