M Pakaski

Summary

Affiliation: University of Szeged
Country: Hungary

Publications

  1. ncbi Vulnerability of small GABAergic neurons to human beta-amyloid pentapeptide
    M Pakaski
    Alzheimer s Disease Research Centre, Albert Szent Gyorgyi Medical University, Szeged, Hungary
    Brain Res 796:239-46. 1998
  2. doi Interactions between the amyloid and cholinergic mechanisms in Alzheimer's disease
    Magdolna Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Semmelweis 6, Szeged H 6725, Hungary
    Neurochem Int 53:103-11. 2008
  3. ncbi Imipramine and citalopram facilitate amyloid precursor protein secretion in vitro
    Magdolna Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Semmelweis 6, H 6725 Szeged, Hungary
    Neurochem Int 47:190-5. 2005
  4. doi Capsaicin promotes the amyloidogenic route of brain amyloid precursor protein processing
    Magdolna Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, 6 Semmelweis, H 6725 Szeged, Hungary
    Neurochem Int 54:426-30. 2009
  5. ncbi Role of acetylcholinesterase inhibitors in the metabolism of amyloid precursor protein
    M Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, Albert Szent Györgyi Center for Medical and Pharmaceutical Sciences, Faculty of Medicine, University of Szeged, Hungary
    Curr Drug Targets CNS Neurol Disord 2:163-71. 2003
  6. ncbi Human amyloid-beta causes changes in the levels of endothelial protein kinase C and its alpha isoform in vitro
    Magdolna Pakaski
    Department of Psychiatry, Alzheimer s Disease Research Centre, University of Szeged, Somogyi 4, H 6720 Szeged, Hungary
    Neurochem Int 41:409-14. 2002
  7. ncbi Reversible and irreversible acetylcholinesterase inhibitors cause changes in neuronal amyloid precursor protein processing and protein kinase C level in vitro
    M Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Somogyi 4, H 6720, Szeged, Hungary
    Neurochem Int 38:219-26. 2001
  8. ncbi In vitro effects of metrifonate on neuronal amyloid precursor protein processing and protein kinase C level
    M Pakaski
    Alzheimer s Disease Research Centre, University of Szeged, 4 Somogyi St, H 6720, Szeged, Hungary
    Brain Res 863:266-70. 2000
  9. ncbi Presenilin-1 and its N-terminal and C-terminal fragments are transported in the sciatic nerve of rat
    P Kasa
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Somogyi B ut 4, H 6720, Szeged, Hungary
    Brain Res 909:159-69. 2001
  10. ncbi Unchanged rat brain amyloid precursor protein levels after exposure to benzodiazepines in vivo
    J Kalman
    University of Szeged, Department of Psychiatry, Hungary
    Eur J Anaesthesiol 23:772-5. 2006

Collaborators

Detail Information

Publications14

  1. ncbi Vulnerability of small GABAergic neurons to human beta-amyloid pentapeptide
    M Pakaski
    Alzheimer s Disease Research Centre, Albert Szent Gyorgyi Medical University, Szeged, Hungary
    Brain Res 796:239-46. 1998
    ..The results suggest that fragments of A beta shorter than A beta 25-35 may exert cytotoxic action and demonstrate the toxicity of these A beta fragments in decreasing the number of small GABAergic neurons...
  2. doi Interactions between the amyloid and cholinergic mechanisms in Alzheimer's disease
    Magdolna Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Semmelweis 6, Szeged H 6725, Hungary
    Neurochem Int 53:103-11. 2008
    ..Further work is warranted to elucidate the exact effects in the interactions between the cholinergic and amyloid hypotheses of the candidate drugs used in AD therapy...
  3. ncbi Imipramine and citalopram facilitate amyloid precursor protein secretion in vitro
    Magdolna Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Semmelweis 6, H 6725 Szeged, Hungary
    Neurochem Int 47:190-5. 2005
    ..Since the secreted APP is not further available for the pathological cleavage of beta- and gamma-secretases, antidepressant medication might be beneficial in AD therapy...
  4. doi Capsaicin promotes the amyloidogenic route of brain amyloid precursor protein processing
    Magdolna Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, 6 Semmelweis, H 6725 Szeged, Hungary
    Neurochem Int 54:426-30. 2009
    ..These in vivo data indicate that capsaicin is able to interfere with the brain APP metabolism by promoting the amyloidogenic route. We suggest that PKC is not involved in the mechanism underlying the effects...
  5. ncbi Role of acetylcholinesterase inhibitors in the metabolism of amyloid precursor protein
    M Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, Albert Szent Györgyi Center for Medical and Pharmaceutical Sciences, Faculty of Medicine, University of Szeged, Hungary
    Curr Drug Targets CNS Neurol Disord 2:163-71. 2003
    ..Further work is warranted to elucidate the exact roles in APP metabolism of the AChE inhibitors used in AD therapy at present...
  6. ncbi Human amyloid-beta causes changes in the levels of endothelial protein kinase C and its alpha isoform in vitro
    Magdolna Pakaski
    Department of Psychiatry, Alzheimer s Disease Research Centre, University of Szeged, Somogyi 4, H 6720 Szeged, Hungary
    Neurochem Int 41:409-14. 2002
    ..These data suggest that the accumulation of A(beta) peptide in the cerebral vasculature may play a significant role in the down-regulation of PKC seen in the AD cerebral vasculature...
  7. ncbi Reversible and irreversible acetylcholinesterase inhibitors cause changes in neuronal amyloid precursor protein processing and protein kinase C level in vitro
    M Pakaski
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Somogyi 4, H 6720, Szeged, Hungary
    Neurochem Int 38:219-26. 2001
    ....
  8. ncbi In vitro effects of metrifonate on neuronal amyloid precursor protein processing and protein kinase C level
    M Pakaski
    Alzheimer s Disease Research Centre, University of Szeged, 4 Somogyi St, H 6720, Szeged, Hungary
    Brain Res 863:266-70. 2000
    ....
  9. ncbi Presenilin-1 and its N-terminal and C-terminal fragments are transported in the sciatic nerve of rat
    P Kasa
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Somogyi B ut 4, H 6720, Szeged, Hungary
    Brain Res 909:159-69. 2001
    ..These results lend further support to the suggestion that presenilin-1 may leave the trans-Golgi network and be found in the axons and axon terminals of the various neurons...
  10. ncbi Unchanged rat brain amyloid precursor protein levels after exposure to benzodiazepines in vivo
    J Kalman
    University of Szeged, Department of Psychiatry, Hungary
    Eur J Anaesthesiol 23:772-5. 2006
    ..Since amyloid precursor protein and its neurotoxic derivatives play key roles in the development of Alzheimer's dementia, the impact of several agents used in the intra- and perioperative period is examined...
  11. ncbi Presenilin-1 and the amyloid precursor protein are transported bidirectionally in the sciatic nerve of adult rat
    H Papp
    Department of Psychiatry, Alzheimer s Disease Research Centre, University of Szeged, Somogyi B ut 4, H 6720 Szeged, Hungary
    Neurochem Int 41:429-35. 2002
    ..It is concluded that the functions of presenilin-1 and APPs are not restricted to the neuronal perikarya: they may carry information in both directions, from the cell body to the axon terminals and vice versa...
  12. ncbi Decreased expression of kynurenine aminotransferase-I (KAT-I) in the substantia nigra of mice after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment
    E Knyihar-Csillik
    Department of Neurology, Albert Szent Gyorgyi Medical School, University of Szeged, Semmelweis u 6, H 6701 Szeged, Hungary
    Neuroscience 126:899-914. 2004
    ..We conclude that MPTP treatment may have a dual effect: in addition to being deleterious for neurons expressing TH and KAT-I, it also affects glial cells which could exacerbate the neurodegenerative process characterizing PD...
  13. ncbi Gene expression profile analysis of lymphocytes from Alzheimer's patients
    J Kalman
    Department of Psychiatry, Albert Szent Györgyi Center for Medical and Pharmaceutical Sciences, Faculty of Medicine, University of Szeged, Semmelweis u 6 H 6725 Szeged, Hungary
    Psychiatr Genet 15:1-6. 2005
    ..It remains to be elucidated, however, how these genes are related to the pathomechanism of dementia and whether the gene expression differences of AD lymphocytes reflect disease traits or stage processes...
  14. ncbi Effects of amyloid-beta on cholinergic and acetylcholinesterase-positive cells in cultured basal forebrain neurons of embryonic rat brain
    Peter Kasa
    Alzheimer s Disease Research Centre, Department of Psychiatry, University of Szeged, Somogyi B ut 4, Szeged H 6720, Hungary
    Brain Res 998:73-82. 2004
    ..It is concluded that the neurotoxic effects of A beta appear more rapidly in the cholinergic axon terminals than in the cholinergic and acetylcholinesterase-positive neuronal perikarya...