Fas and Fas ligand expression in Alzheimer's disease
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Fas and Fas ligand expression in Alzheimer's disease. / Ferrer, I; Puig, B; Krupinsk, J; Carmona, M; Blanco, R; Puig Martorell, Berta.
in: ACTA NEUROPATHOL, Jahrgang 102, Nr. 2, 01.08.2001, S. 121-31.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Fas and Fas ligand expression in Alzheimer's disease
AU - Ferrer, I
AU - Puig, B
AU - Krupinsk, J
AU - Carmona, M
AU - Blanco, R
AU - Puig Martorell, Berta
PY - 2001/8/1
Y1 - 2001/8/1
N2 - The Fas/Fas ligand (L) signaling system has been implicated in the control of cell death and cell survival of T and B lymphocytes and in a variety of cell types under particular pathological conditions. In the present study we examined the expression of Fas and Fas-L, by Western blotting and immunohistochemistry, in the human frontal cortex and hippocampus of individuals with advanced Alzheimer's disease (AD) and age-matched controls. Expression levels of Fas and Fas-L, as seen in Western blots, are preserved in the frontal cortex but decreased in the hippocampus in AD when compared with age-matched controls. Yet Fas and Fas-L immunoreactivity is found in remaining AD neurons in the frontal cortex and hippocampus. Moreover, Fas and Fas-L are expressed equally in tangle-bearing and non-tangle-bearing neurons, as revealed with double-labeling immunohistochemistry to Fas or Fas-L and tau or phosphorylated neurofilament epitopes. Dystrophic neurites of senile plaques are not stained with Fas and Fas-L antibodies. A moderate increase in Fas and a strong increase in Fas-L immunoreactivity occur in reactive astrocytes in AD. Yet there is no relationship between Fas or Fas-L expression and increased nuclear DNA vulnerability as revealed with double-labeling immunohistochemstry and in situ end-labeling of nuclear DNA fragmentation. Although the Fas/Fas-L system may have some effect in the control of reactive astrocytosis in AD, the present results show no evidence that Fas/Fas-L signals participate in specific processes of the disease, including neurofibrillary degeneration, dystrophic neurite formation, and cell death.
AB - The Fas/Fas ligand (L) signaling system has been implicated in the control of cell death and cell survival of T and B lymphocytes and in a variety of cell types under particular pathological conditions. In the present study we examined the expression of Fas and Fas-L, by Western blotting and immunohistochemistry, in the human frontal cortex and hippocampus of individuals with advanced Alzheimer's disease (AD) and age-matched controls. Expression levels of Fas and Fas-L, as seen in Western blots, are preserved in the frontal cortex but decreased in the hippocampus in AD when compared with age-matched controls. Yet Fas and Fas-L immunoreactivity is found in remaining AD neurons in the frontal cortex and hippocampus. Moreover, Fas and Fas-L are expressed equally in tangle-bearing and non-tangle-bearing neurons, as revealed with double-labeling immunohistochemistry to Fas or Fas-L and tau or phosphorylated neurofilament epitopes. Dystrophic neurites of senile plaques are not stained with Fas and Fas-L antibodies. A moderate increase in Fas and a strong increase in Fas-L immunoreactivity occur in reactive astrocytes in AD. Yet there is no relationship between Fas or Fas-L expression and increased nuclear DNA vulnerability as revealed with double-labeling immunohistochemstry and in situ end-labeling of nuclear DNA fragmentation. Although the Fas/Fas-L system may have some effect in the control of reactive astrocytosis in AD, the present results show no evidence that Fas/Fas-L signals participate in specific processes of the disease, including neurofibrillary degeneration, dystrophic neurite formation, and cell death.
KW - Aged
KW - Alzheimer Disease
KW - Animals
KW - Antigens, CD95
KW - Astrocytes
KW - Blotting, Western
KW - DNA Fragmentation
KW - Fas Ligand Protein
KW - Female
KW - Frontal Lobe
KW - Gene Expression
KW - Hippocampus
KW - Humans
KW - Immunohistochemistry
KW - In Situ Nick-End Labeling
KW - Infarction, Middle Cerebral Artery
KW - Male
KW - Membrane Glycoproteins
KW - Middle Aged
KW - Neurofibrillary Tangles
KW - Neurons
KW - Plaque, Amyloid
KW - Rats
KW - Rats, Sprague-Dawley
KW - Signal Transduction
KW - Subcellular Fractions
M3 - SCORING: Journal article
C2 - 11563626
VL - 102
SP - 121
EP - 131
JO - ACTA NEUROPATHOL
JF - ACTA NEUROPATHOL
SN - 0001-6322
IS - 2
ER -