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Pancreatic cells can be converted to hepatocytes by overexpression of C/EBPbeta (Shen, C-N, Slack, J.M.W. and Tosh, D., 2000. Molecular basis of transdifferentiation of pancreas to liver. Nature Cell Biology 2: 879-887). This suggested that expression of one or more C/EBP factors may distinguish liver and pancreas in early development. We have now studied the early expression of C/EBPalpha and C/EBPbeta in the mouse embryo and show that both are expressed exclusively in the early liver bud and not in the pancreatic buds. Their expression is identical to that of hepatocyte nuclear factor 4 (HNF4), another key hepatic transcription factor and alpha-fetoprotein (AFP), a differentiation product characteristic of immature hepatocytes. Both are complementary to the early expression of Pdx1, a key pancreatic transcription factor. These results are consistent with the idea that C/EBP factors are master regulators for liver development.

Pancreatic cells can be converted to hepatocytes by overexpression of C/EBPbeta (Shen, C-N, Slack, J.M.W. and Tosh, D., 2000. Molecular basis of transdifferentiation of pancreas to liver. Nature Cell Biology 2: 879-887). This suggested that expression of one or more C/EBP factors may distinguish liver and pancreas in early development. We have now studied the early expression of C/EBPalpha and C/EBPbeta in the mouse embryo and show that both are expressed exclusively in the early liver bud and not in the pancreatic buds. Their expression is identical to that of hepatocyte nuclear factor 4 (HNF4), another key hepatic transcription factor and alpha-fetoprotein (AFP), a differentiation product characteristic of immature hepatocytes. Both are complementary to the early expression of Pdx1, a key pancreatic transcription factor. These results are consistent with the idea that C/EBP factors are master regulators for liver development.

The brains of people with Alzheimer's disease (AD) display several characteristic pathological features, including deposits (plaques) of beta-amyloid 1-42 (Abeta1-42), intraneuronal accumulations (tangles) of hyperphosphorylated tau, degeneration of the basal forebrain cholinergic pathway, and gliosis. Abeta1-42 plaques develop in specific brain regions, including hippocampus and cortex, as well as in the vasculature. Abeta1-42 might promote neurodegeneration through the induction of free radicals and disruption of Ca2+ homeostasis, giving rise to the symptoms of AD. Abeta1-42 interacts with the alpha7 subtype of the nicotinic acetylcholine receptor (alpha7 nAChR), which is widely expressed throughout the central and peripheral nervous systems, as well as in several nonneuronal loci, such as epithelial cells, lymphoid tissues, and peripheral blood lymphocytes. Western blot and autoradiographic analyses indicate that the alpha7 nAChR subunit protein is up-regulated in human brain samples from Alzheimer patients, as well as in animal models of AD (Dineley et al., 2001; Bednar et al., 2002), and might be involved in nicotine-mediated reduction of Abeta1-42 deposition (Hellstrom et al., 2004), although the nature of this relationship remains ill-defined. We have undertaken a semiquantitative histological evaluation of alpha7 nAChR expression in a mouse model of AD pathology, as well as a comparison of alpha7 nAChR levels in lymphocytes from AD patients and control subjects.

The brains of people with Alzheimer's disease (AD) display several characteristic pathological features, including deposits (plaques) of beta-amyloid 1-42 (Abeta1-42), intraneuronal accumulations (tangles) of hyperphosphorylated tau, degeneration of the basal forebrain cholinergic pathway, and gliosis. Abeta1-42 plaques develop in specific brain regions, including hippocampus and cortex, as well as in the vasculature. Abeta1-42 might promote neurodegeneration through the induction of free radicals and disruption of Ca2+ homeostasis, giving rise to the symptoms of AD. Abeta1-42 interacts with the alpha7 subtype of the nicotinic acetylcholine receptor (alpha7 nAChR), which is widely expressed throughout the central and peripheral nervous systems, as well as in several nonneuronal loci, such as epithelial cells, lymphoid tissues, and peripheral blood lymphocytes. Western blot and autoradiographic analyses indicate that the alpha7 nAChR subunit protein is up-regulated in human brain samples from Alzheimer patients, as well as in animal models of AD (Dineley et al., 2001; Bednar et al., 2002), and might be involved in nicotine-mediated reduction of Abeta1-42 deposition (Hellstrom et al., 2004), although the nature of this relationship remains ill-defined. We have undertaken a semiquantitative histological evaluation of alpha7 nAChR expression in a mouse model of AD pathology, as well as a comparison of alpha7 nAChR levels in lymphocytes from AD patients and control subjects.