Fas and Fas ligand expression in Alzheimer's disease

TY - JOUR

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 -