| Abstract No.: | B-C2083 |
| Country: | Canada |
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| Title: | INCREASED NUMBER OF APOPTOSIS-INDUCING FACTOR (AIF)-IMMUNOREACTIVE NEURONS IN THE HIPPOCAMPUS IN ALZHEIMER'S DISEASE |
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| Authors/Affiliations: | 1 Wenfeng Yu*; 1 Naguib Mechawar; 2 Slavica Krantic; 1 Rémi Quirion;
1 Douglas Mental Health University Institute, Montreal, QC, Canada; 2 INMED, INSERM U29, Luminy, Marseille, France
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| Content: | Objective: Programmed cell death (PCD) is likely contributed to neuronal loss in the brain of AlzheimerˇÇs disease (AD) via caspase-dependent and -independent pathways. The mitochondrial flavoprotein, apoptosis-inducing factor (AIF) is a major caspase-independent death-effector molecule. Upon apoptogenic insult, AIF is released from mitochondria and further translocated to the nucleus, where it is associated with high molecular weight DNA fragmentation, chromatin condensation and cell death (Krantic et al. 2007. Prog Neurobiol 81:179-96). AlzheimerˇÇs disease (AD) is the most common neurodegenerative disorder, and is characterized by a progressive impairment of cognition and emotional disturbances that are strongly correlated with synaptic degeneration and neuronal death in limbic structures. Although caspase-dependent cell death has been involved in AD (LeBlanc. 2005. Curr Alzheimer Res. 2: 389-402), little is known about the mechanisms involved in the regulation of caspase-independent pathway in AD–associated neuronal death. We have recently found no difference in cortical and hippocampal AIF levels between AD and age-matched control subjects (Reix et al. 2007. Neurobiol Aging 28:351-6). In the present study, the distribution of AIF-immunoreactive cells in the frontal cortex and hippocampus are compared between AD and age-matched control brains.
Materials and Methods: The immunocytochemical distribution of AIF was investigated in the hippocampus and frontal cortex of normal subjects of various ages and subjects with AD using immunocytochemical staining as previous described (Yu et al. 2005. Exp Neurol 192: 215-25). The total number of neurons was evaluated by Nissl staining in the adjacent brain sections.
Results: AIF-immunoreactivity was mainly seen in neurons and much less in astrocytes and microglia in both brain regions. In AD versus controls, a significant increase in the number of AIF-immunoreactive (-IR) neurons was quantified in the CA1 and CA2 fields of the hippocampus.
Conclusion: The observed increase in the number of AIF-IR neurons in the AD hippocampus suggests a more widespread involvement of the caspase-independent PCD pathway in AD-related PCD. Supported by CIHR |
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