TY  - JOUR
A1  - Schindowski, Katharina
A1  - Kratzsch, Tilmann
A1  - Peters, Jürgen
A1  - Steiner, Barbara
A1  - Leutner, Silke
A1  - Touchet, Natalie
A1  - Maurer, Konrad
A1  - Czech, Christian
A1  - Pradier, Laurent
A1  - Frölich, Lutz
A1  - Müller, Walter E.
A1  - Eckert, Anne
T1  - Impact of aging : sporadic, and genetic risk factors on vulnerability to apoptosis in Alzheimer's disease
T2  - Neuromolecular Medicine
N2  - 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.
KW  - transgenic mice
KW  - presenilin-1
KW  - amyloid precursor protein (APP)
KW  - lymphocytes
KW  - AD patients
KW  - apoptosis
Y1  - 2006
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/1967
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30-34471
UR  - http://journals.humanapress.com
VL  - 4
IS  - 3
SP  - 161
EP  - 178
ER  -