Eradication of Helicobacter pylori may be beneficial in the management of Alzheimer’s disease. J Neurol
ABSTRACT Infectious agents have been proposed as potential causes of Alzheimer's disease (AD). Recently, we documented a high prevalence of Helicobacter pylori (Hp) infection in patients with AD. We aim to access the effect of Hp eradication on the AD cognitive (MMSE: Mini Mental State Examination and CAMCOG: Cambridge Cognitive Examination for the Elderly) and functional (FRSSD: Functional Rating Scale for Symptoms of Dementia) status parameters. In the first part of the study, a total of 50 consecutive patients with AD and 30 age-matched anaemic controls underwent an upper gastrointestinal endoscopy, and gastric mucosal biopsies were obtained to detect the presence of Hp infection by histologic analysis and rapid urease test. Serum anti-Hp-specific IgG level was analysed by enzyme-linked immunosorbent assay. In the second part, Hp-positive AD patients received a triple eradication regimen (omeprazole, clarithromycin and amoxicillin), and all patients were followed up for 2 years, while under the same treatment with cholinesterase inhibitors. Hp was detected in 88% of AD patients and in 46.7% of controls (P < 0.001). Hp eradication was successful in 84.8% of treated patients. At the 2-year clinical endpoint, cognitive and functional status parameters improved in the subgroup of patients where Hp eradication was successful (P < 0.001 and P = 0.049 for MMSE and CAMCOG, respectively; P < 0.001 for FRSSD), but not in the other patients. Hp eradication may positively influence AD manifestations, suggesting a possible common link between Hp and AD.
- SourceAvailable from: Mohammed Al-Qahtani
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- "Using some histological studies it was found that there is an association between H. pylori and AD . Furthermore, eradication of H. pylori from AD patients positively influences cognitive and functional status of patient . In a recent study it has been reported that H. pylori infection triggers accumulation of AD lesions and neuroinflammation hence is a significant risk factor for developing AD . "
ABSTRACT: Alzheimer disease (AD) is a degenerative disease of brain that is associated with dementia, brain atrophy, accumulation of hyperphosphorylated tau protein and amyloid-beta peptide in hippocampus and cortex region of the brain. The development of AD is a multifactorial process that may also involve infection with bacterial pathogens. Recent studies suggest that bacteria including spirochetes have potential to initiate cascade of events leading to inflammatory condition of central nervous system. Bacteria and spirochetes are activators of proinflammatory cytokines, generate free radicals, nitric oxide and further induction of apoptosis. Infection with these microbes may be considered as a risk factor for pathophysiology of AD or to cognitive changes. Recent studies have revealed that exposure to these microorganisms induces Aβ accumulation and tau protein phosphorylation and chronic infection with these pathogenic bacteria can possibly contribute to progression of AD. In this article, we update and review the role of bacteria in the pathogenesis of AD resulting from initiation of cascade events in chronic inflammations and amyloidogenesis. By controlling these chronic infections with antibacterial or anti-inflammatory drugs will allow preventing inflammation, a risk factor for AD.CNS & Neurological Disorders - Drug Targets (Formerly Current Drug Targets - CNS & Neurological Disorders) 09/2014; 13(7). DOI:10.2174/1871527313666140917115741 · 2.70 Impact Factor
Conference Paper: A land cover monitoring system for Cambodia: preliminary results[Show abstract] [Hide abstract]
ABSTRACT: A monitoring system using coarse satellite data integrated into a geographic information system (GIS) has been developed to assess the land cover change in Cambodia. The present case study focuses on the assessment of land cover variables involving the issues of deforestation, slash and burn practices and variation in water levels of the Tonle Sap lake. The baseline of the monitoring is defined from the comparison of the existing maps. The NOAA AVHRR data provide the information on an annual basis for the vegetation variable and every two months for the water-level variable. The main mapping outputs are an updated version of the evergreen forest map and the map of the burnt areas of Cambodia. Valuable information has also been found at the seasonal and annual scale of the water-level change of the Tonle SapGeoscience and Remote Sensing Symposium, 1993. IGARSS '93. Better Understanding of Earth Environment., International; 09/1993
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ABSTRACT: Helicobacter pylori (H. pylori) infection is a chronic gastric Gram-negative infection that increases with age. Acquired in childhood, H. pylori infection may induce a whole cascade of events leading to gastric pathologies such as peptic ulcer diseases, gastric precancerous lesions, and gastric lymphomas (MALT). The characteristics of the diagnosis and the treatment of this infection in geriatrics are thus particularly important to take into account. 1) The incidence of gastric and duodenal ulcers and their bleeding complications is increasing in old-aged populations. Clinical signs such as anorexia and malnutrition are proven to be excellent indications for endoscopic explorations in the elderly. NSAID-use and H. pylori infection were shown to be independent and unrelated risk factors for peptic ulcer and gastroduodenal bleeding in elderly subjects; 2) H. pylori infection diagnosis is difficult to realize in the very old population, and the urea breath test is the test which obtain the best performances in this population. Recent work showed the part played by H. pylori chronic infection in gastric aging and in appetite regulation in the elderly. Research tasks should be continued in this field in order to better understand the part played by this chronic infection in gastric aging and in other pathologies (i.e. neurological or cardiovascular diseases) in this population.La Revue de Médecine Interne 07/2007; 28(6):400-11. DOI:10.1016/j.revmed.2007.01.017 · 1.32 Impact Factor