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Biomedical subjects

Dimitrios Chatzopoulos

Publications and source records attributed to Dimitrios Chatzopoulos.

At least 19 recordsLinked to original sources
PubMed2006

Alzheimer's disease and Helicobacter pylori infection: Defective immune regulation and apoptosis as proposed common links.

Although degenerative diseases of the central nervous system, including Alzheimer's disease (AD), have an increasingly high impact on aged population their association with Helicobacter pylori (H. pylori) infection has not as yet been thoroughly researched. Current H. pylori infection appears to induce irregular humoral and cellular immune responses that, owing to the sharing of homologous epitopes (molecular mimicry), cross-react with components of nerves, thereby contributing and possibly perpetuating the apoptotic neural tissue damage observed in neurodegenerative diseases including AD. An association between AD and H. pylori infection has been recently addressed by two studies. A higher seropositivity for anti-H. pylori immunoglobulin G antibodies in 30 patients with AD than in 30 age-matched controls was reported in one study; this serological test, however, has limitations because it does not discriminate between current and old infections. In the other study, by introducing the histological method (the actual gold standard) for diagnosis of H. pylori infection, we reported a higher prevalence of H. pylori infection in 50 AD patients than in 30 anemic controls. This pathogen may influence the pathophysiology of AD by promoting platelet and platelet-leukocyte aggregation; releasing various pro-inflammatory and vasoactive substances; developing cross-mimicry with host antigens; producing reactive oxygen metabolites and circulating lipid peroxides; influencing the apoptotic process; and increasing, through induction of atrophic gastritis, homocysteine, which contributes to vascular disorders implicated in endothelial damage and neurodegeneration.

Alzheimer Disease↗
PubMed2005

Apoptotic and anti-angiogenic strategies in liver and gastrointestinal malignancies.

Inappropriate suppression of apoptosis is strongly implicated in tumorigenesis. Tumor development is heralded by the mutation of tumor suppressor genes and overexpression of anti-apoptotic genes permitting cell survival. Thus, inducing the apoptotic process in various ways can be applied to cancer management. Besides, angiogenesis is a crucial process for tumor growth and metastasis. New strategies targeting fundamental play-markers of the angiogenic process are currently under investigation.

Angiogenesis Inhibitors↗
PubMed2005

New molecular concepts of Barrett's esophagus: clinical implications and biomarkers.

Barrett's esophagus (BE) represents the most serious histological consequence of gastroesophageal reflux disease (GERD) that develops in 5-10% of patients with GERD. Given that BE is the only known precursor to esophageal adenocarcinoma (EA), a systematic endoscopic biopsy protocol can detect EAs at an early stage. However, endoscopic and histopathological evaluation of BE are not adequate for effective screening of high risk patients. Therefore, molecular abnormalities associated with BE have been considered as surrogate markers and their use as such is proposed. Flow cytometry is the most useful adjunct to histology, and ploidy status of BE is an independent risk factor. Cyclin D1 overexpression is inversely correlated with survival in EA. C-erbB2 (+) patients have poorer prognosis. High plasma adenomatous polyposis coli levels correlate with reduced patient survival. p53 expression allows patient risk for EA stratification. Nuclear factor-kappaB overexpression inversely correlates with good response to adjuvant chemotherapy and radiotherapy in EA. Patients with cyclooxygenase-2 overexpression have reduced survival rates. Increased E-cadherin staining is associated with shorter survival in EA patients who received chemoradiotherapy. Finally, existing data cannot rule out a correlation between EA and colorectal tumors. Seventeen BE molecular alterations yielded noteworthy clinical implications. Apart from endoscopy and histology, these data allow for better risk stratification for patients with BE and for more efficient and timely therapeutic approaches.

Adenocarcinoma↗
PubMed2004

Induction of apoptosis as a proposed pathophysiological link between glaucoma and Helicobacter pylori infection.

Although apoptosis is equally important both for the development and for the maintenance of homeostasis in some adult tissues, it can also be associated with disease processes. Current studies indicate that apoptosis is a mechanism of cell death in several important ocular and gastrointestinal diseases including glaucoma, and Helicobacter pylori (H. pylori)-induced upper gastrointestinal disorders and/or extraintestinal diseases, including autoimmune and neurodegenerative ones (Sjögren's syndrome, Guillain-Barre syndrome or Parkinson's disease). Glaucoma is also associated with similar autoimmune and neurodegenerative disorders, characterized by apoptotic loss of specific populations of neurons. Recently, a high prevalence of H. pylori infection has been recognized in patients with chronic open-angle glaucoma. In addition, H. pylori eradication may positively influence glaucoma parameters, thereby suggesting a possible causal link between H. pylori and glaucoma. H. pylori infection may influence the pathophysiology of glaucoma by releasing various proinflammatory and vasoactive substances, as well as by influencing apoptotic process; parameters that may also exert their own effects in the induction and/or progression of glaucomatous neuropathy. Importantly, H. pylori infection and glaucoma share the Fas/FasL and the mitochondria-mediated apoptotic pathways, thereby proposing an apoptotic link in the pathophysiology of both diseases.

Apoptosis↗
PubMed2004

Apoptosis and autoimmunity as proposed pathogenetic links between Helicobacter pylori infection and idiopathic achalasia.

Achalasia is a disorder of the oesophagus characterised by increased lower oesophageal sphincter (LOS) tone, lack of LOS relaxation with swallowing and aperistalsis of the body of the oesophagus. The aetiology and pathogenesis of idiopathic achalasia are still unclear, although a viral cause, genetic influences (associations with HLA loci) and autoimmune processes have been postulated. Degeneration and significant loss of nerve fibres, associated with an inflammatory infiltrate of the myenteric plexus in idiopathic achalasia, provide evidence of an immune mediated destruction of the myenteric plexus, possibly through apoptotic process. This concept is reinforced by the concomitant appearance of achalasia and Guillain-Barré syndrome (GBS) and/or Parkinson's disease, where inappropriate initiation of apoptosis has been proposed to underlie the neuronal attrition. In the same respect, Helicobacter pylori (H. pylori) infection has been associated with gastric autoimmunity, and patients infected with H. pylori have been shown to possess autoantibodies that cross-react with antigens expressed on the gastric mucosa. Furthermore, H. pylori is thought to be associated with the development of autoimmune sequelae observed in peripheral neuropathies and GBS, where autoantibodies to specific neural targets have been found to impair native neural function by inducing nerve tissue damage, possibly by apoptosis. Taken together, we assume that H. pylori infection might be a pathogenetic factor of achalasia through induction of autoimmunity and apoptosis. Whether eradication of H. pylori infection may indirectly offer benefit to the pathophysiology of idiopathic achalasia by ameliorating the apoptotic loss of ganglion cells and their axons in the oesophageal wall remains to be elucidated.

Animals↗