Lymphocytes and neutrophils as peripheral models to study the effect of beta-amyloid on cellular calcium signalling in Alzheimer's disease

Eckert, A. and Förstl, H. and Zerfass, R. and Hartmann, H. and Müller, W. E.. (1996) Lymphocytes and neutrophils as peripheral models to study the effect of beta-amyloid on cellular calcium signalling in Alzheimer's disease. Life sciences, Vol. 59, no. 5-6. pp. 499-510.

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Official URL: http://edoc.unibas.ch/dok/A5253512

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According to the calcium hypothesis of brain aging, disturbances of free intracellular calcium homeostasis ([Ca2+]i) play a key role in pathology of Alzheimer's disease (AD). Recent data from neuronal tissue culture support the contribution of the beta-amyloid peptide (beta A) to neurodegeneration in AD, probably by disruption of the intracellular Ca2+ regulation. On the basis of this premise, we used peripheral blood cells to examine the role of beta A on Ca2+ signalling, not only to obtain an experimental approach to investigate these effects of beta A in man, but also to search for AD-specific alterations of the effects of beta A on Ca2+ signalling. This approach is based on observations indicating that the phytohemagglutinin (PHA)-induced Ca2+ response in circulating human lymphocytes of healthy volunteers is affected by beta A and its fragment 25-35 in a fashion similar to its effects on central neurons, whereas we found no effect of beta A on receptor-activated Ca2+ response in neutrophils. Therefore, we used human blood lymphocytes as peripheral model systems to search directly for AD-related abnormalities of Ca2+ regulation, for alterations of beta A effects on Ca2+ signalling and on membrane fluidity, and for possible changes of potassium channels. In accordance with our data in neutrophils, we were unable to identify any relevant change of the PHA-induced Ca2+ elevations in lymphocytes, which is not supporting the assumption of general alterations of cellular Ca2+ regulation in AD. On the other hand, the amplifying effect of beta A on Ca2+ signalling was significantly reduced in lymphocytes from AD patients. Moreover, Ca2+ responses to beta A25-35 were not different between early- and late-onset AD patients. Our findings indicate that the sensitivity of the lymphocyte for the effects of beta A is reduced in a high percentage of patients with probable or possible AD. As possible explanation we observed a similar reduction of the sensitivity of the ly
Faculties and Departments:03 Faculty of Medicine > Bereich Psychiatrie (Klinik) > Erwachsenenpsychiatrie UPK
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Psychiatrie (Klinik) > Erwachsenenpsychiatrie UPK
UniBasel Contributors:Eckert, Anne
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Elsevier Science
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:22 Mar 2012 14:23
Deposited On:22 Mar 2012 13:35

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