Literature DB >> 12515309

Whole blood samples from Alzheimer patients and control donors demonstrate fluorimetric differences.

András Palotás1, János Kálmán, Miklós Palotás, Keyvan Matin, Károly Szentpáli, Attila Paszt, Zoltán Janka, Botond Penke.   

Abstract

Beta-amyloid peptide plays a crucial role in the pathology of Alzheimer's disease. As part of our ongoing fluorimetric studies, in the present report we demonstrate differences in resting intracellular free calcium levels of cells in the blood derived from sporadic Alzheimer patients and from age-matched control individuals. Calcium levels were measured in Fura-2AM-loaded human blood samples by dual-wavelength spectrofluorimetry. The resting calcium concentrations of blood samples from Alzheimer patients were lower compared to that of the control samples. Exposure of control blood samples to beta-amyloid caused an increase in the calcium level. Specimens from Alzheimer donors, however, appeared to be resistant to the peptide. This simple finding may serve as a springboard to monitoring Alzheimer pathology in the peripheral systems of the body.

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Year:  2002        PMID: 12515309     DOI: 10.1023/a:1021618523577

Source DB:  PubMed          Journal:  Neurochem Res        ISSN: 0364-3190            Impact factor:   3.996


  11 in total

1.  Protein measurement with the Folin phenol reagent.

Authors:  O H LOWRY; N J ROSEBROUGH; A L FARR; R J RANDALL
Journal:  J Biol Chem       Date:  1951-11       Impact factor: 5.157

2.  Calcium mobilization evoked by amyloid beta-protein involves inositol 1,4,5-triphosphate production in human platelets.

Authors:  H Ishikawa; H Ozawa; T Saito; N Takahata; H Takemura
Journal:  Life Sci       Date:  1998       Impact factor: 5.037

3.  Plasma and erythrocyte acetylcholinesterase in senile dementia of Alzheimer type.

Authors:  R H Perry; I D Wilson; M J Bober; J Atack; G Blessed; B E Tomlinson; E K Perry
Journal:  Lancet       Date:  1982-01-16       Impact factor: 79.321

4.  beta-Amyloid peptide decreases membrane fluidity.

Authors:  W E Müller; S Koch; A Eckert; H Hartmann; K Scheuer
Journal:  Brain Res       Date:  1995-03-13       Impact factor: 3.252

5.  Comparative studies on [Ca2+]i-level of fibroblasts from Alzheimer patients and control individuals.

Authors:  A Palotás; J Kálmán; G Laskay; A Juhász; Z Janka; B Penke
Journal:  Neurochem Res       Date:  2001-07       Impact factor: 3.996

Review 6.  Calcium alterations in Alzheimer's disease: pathophysiology, models and therapeutic opportunities.

Authors:  A Pascale; R Etcheberrigaray
Journal:  Pharmacol Res       Date:  1999-02       Impact factor: 7.658

Review 7.  beta-Amyloid precursor protein metabolites and loss of neuronal Ca2+ homeostasis in Alzheimer's disease.

Authors:  M P Mattson; S W Barger; B Cheng; I Lieberburg; V L Smith-Swintosky; R E Rydel
Journal:  Trends Neurosci       Date:  1993-10       Impact factor: 13.837

Review 8.  Fibroblast models of neurological disorders: fluorescence measurement studies.

Authors:  G P Connolly
Journal:  Trends Pharmacol Sci       Date:  1998-05       Impact factor: 14.819

9.  Fibroblasts and lymphocytes from Alzheimer patients are resistant to beta-amyloid-induced increase in the intracellular calcium concentration.

Authors:  András Palotás; János Kálmán; Miklós Palotás; Anna Juhász; Zoltán Janka; Botond Penke
Journal:  Prog Neuropsychopharmacol Biol Psychiatry       Date:  2002-06       Impact factor: 5.067

10.  beta-Amyloid peptides enhance binding of the calcium mobilising second messengers, inositol(1,4,5)trisphosphate and inositol-(1,3,4,5)tetrakisphosphate to their receptor sites in rat cortical membranes.

Authors:  R F Cowburn; B Wiehager; E Sundström
Journal:  Neurosci Lett       Date:  1995-05-19       Impact factor: 3.046

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