Alzheimer's factors in postischemic dementia

Vol. 53 No. 3 Suppl., 2012
This supplement was not sponsored by Outside Organizations.


R. Pluta, Marzena Ulamek-Koziol, S. Januszewski, Malgorzata Scislewska, Anna Bogucka-Kocka, J. Kocki

The way for explanation postischemic dementia processes has been one fraught with a wide range of complications and frequent revisions with a lack of a final clear solution. Data from animal models of brain ischemia and human ischemic brains studies have demonstrated an overexpression of amyloid precursor protein and increase production of a beta-amyloid peptide. Restoration brain activity following ischemic brain episode is delayed and not always complete due to an alteration related with increase in the level of the beta-amyloid peptide. In this paper, we will propose our idea about production of the beta-amyloid peptide from the amyloid precursor protein in ischemic brain lesions, and how this protein presents etiological and therapeutic targets that are now under consideration. Maturation of the ischemic brain tissue pathology may be caused not only by a neurodegeneration of selectively vulnerable neuronal cells destroyed following ischemia but also by acute and chronic pathology of resistant parts of the brain and chronic changes in the blood-brain barrier. We propose that in dementia following ischemia an initial ischemic episode precedes the brain tissue deposition of beta-amyloid peptide, which in turn amplifies the vascular dysfunction after first episode of ischemia triggering next focal ischemic episodes as vicious cycle preceding final ischemic degenerative changes and may gradually over a lifetime, progress to brain atrophy and finally to postischemic dementia with Alzheimer's phenotype.

Corresponding author: Ryszard Pluta, Professor, MD, PhD; e-mail:

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Corina Gabriela Cotoi, Shirin Elizabeth Khorsandi, I. E. Plesea, A. Quaglia

Hepatocellular carcinoma (HCC) is the fifth most common type of cancer in men and the seventh in women and is the third most common cause of death from cancer worldwide []. The overall incidence of HCC remains high in developing countries and is steadily rising in most industrialized countries [Shariff MI et al., 2009]. A variety of therapeutic modalities is available for treating hepatocellular carcinoma, but orthotopic liver transplantation (OLT) represents a curative option. Due to the shortage of donor organs and the increasing need for liver transplantation in the last decade, local ablation therapy (LAT) has been increasingly used in many centers as a bridge to transplant [Majno PE et al., 1997; Decaens T et al., 2005; Herber S et al., 2005; Bharat A et al., 2006; Obed A et al., 2007; Otto G et al., 2007]. We retrieved from the archive in the Histopathology Laboratory, Institute of Liver Studies, Kingâ??s College Hospital, London, UK, 28 cases of HCC, which underwent treatment with TACE (Doxorubicin 40 mg/m2) as a bridge to transplantation, between 2008 and 2010. We also analyzed 14 additional post-TACE tumors, classified according to the architectural patterns published by Morisco F et al. (2008), for quantification of necrosis. Extensive tumor necrosis was observed in 12 (42.85%) of the patients. Viable hepatocellular carcinoma showed a wide range of differentiation, from well to poorly differentiated. The phenotype of the tumors was mostly hepatocelluar, but 14% showed a mixed phenotype, including glandular/pseudoglandular formation and cholangiocellular components. The percentage of necrosis ranged between 0% and 100%, with an average of 50.6%. There was no statistical correlation between the total size of the nodules and the surface of necrosis in our series (p=0.125). In conclusion, the systematic pathological assessment of post-TACE resected HCC can help in investigating the biology of treated tumors but needs to incorporate sampling protocols, digital image analysis, phenotypic classification by immunohistochemistry and enzymatic function.

Corresponding author: Corina Gabriela Cotoi, Clinical Research Fellow; e-mail:

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