Impact of aging : sporadic, and genetic risk factors on vulnerability to apoptosis in Alzheimer's disease

The identification of specific genetic (presenilin-1 [PS1] and amyloid precursor protein [APP] mutations) and environmental factors responsible for Alzheimer's disease (AD) has revealed evidence for a shared pathway of n
The identification of specific genetic (presenilin-1 [PS1] and amyloid precursor protein [APP] mutations) and environmental factors responsible for Alzheimer's disease (AD) has revealed evidence for a shared pathway of neuronal death. Moreover, AD-specific cell defects may be observed in many other nonneuronal cells (e.g., lymphocytes). Thus, lymphocytes may serve as a cellular system in which to study risk factors of sporadic, as well as genetic AD in vivo. The aim of our present study was to clarify whether lymphocytes bearing genetic or sporadic risk factors of AD share an increased susceptibility to cell death. Additionally we examined whether a cell typespecific vulnerability pattern was present and how normal aging, the main risk factor of sporadic AD, contributes to changes in susceptibility to cell death. Here, we report that lymphocytes affected by sporadic or genetic APP and PS1 AD risk factors share an increased vulnerability to cell death and exhibit a similar cell type-specific pattern, given that enhanced vulnerability was most strongly developed in the CD4+ T-cell subtype. In this paradigm, sporadic risk factors revealed the highest impact on cell type-specific sensitivity of CD4+ T cells to apoptosis. In contrast, normal aging results in an increased susceptibility to apoptosis of both, CD4+ and CD8+ T cells.
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Metadaten
Author:Katharina Schindowski, Tilmann Kratzsch, Jürgen Peters, Barbara Steiner, Silke Leutner, Natalie Touchet, Konrad Maurer, Christian Czech, Laurent Pradier, Lutz Frölich, Walter E. Müller, Anne Eckert
URN:urn:nbn:de:hebis:30-34471
Document Type:Article
Language:English
Date of Publication (online):2006/11/29
Year of first Publication:2003
Publishing Institution:Univ.-Bibliothek Frankfurt am Main
Release Date:2006/11/29
Tag:AD patients ; amyloid precursor protein (APP) ; apoptosis; lymphocytes ; presenilin-1 ; transgenic mice
Source:In: Neuromolecular Med. 2003;4(3):161-78 ; http://journals.humanapress.com
HeBIS PPN:195728084
Institutes:Pharmazie
Dewey Decimal Classification:570 Biowissenschaften; Biologie
Sammlungen:Universitätspublikationen
Sondersammelgebiets-Volltexte
Licence (German):License Logo Veröffentlichungsvertrag für Publikationen

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