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Fuentes P.,University of Chile | Catalan J.,International Center for Biomedicine
Current Alzheimer Research | Year: 2011

Alzheimer's Disease (AD) physiopathology is not yet totally established. Nevertheless it is known that a metabolism dysfunction of the amyloid beta precursor protein (APP) and the abnormal tau protein phosphorylation lead to the formation of neuritic plaques and neurofibrillary tangles, respectively. These events finally drive to the clinical expression of dementia. Formally approved during the past decade, treatments for AD are lacking of an updating, being essentially symptomatic. Anticholinesterase agents have failed in providing a substantial improvement in the mental health condition of AD patients. On the other hand, antiamyloid strategies, have failed in their efficacy or security on their last development phases. In this context, tau represents a potential therapeutic target, by the action of drugs that diminish its aggregation, or acting by altering its phosphorylation or filaments formation. There is also anti-tau miscellaneous strategies such as normal microtubule-stabilizing agents. Thus, it might be possible that in a near future the neurodegenerative process could be stopped. © 2011 Bentham Science Publishers. Source

Guzman-Martinez L.,University of Chile | Guzman-Martinez L.,International Center for Biomedicine | Farias G.A.,International Center for Biomedicine | Maccioni R.B.,University of Chile | Maccioni R.B.,International Center for Biomedicine
Archives of Medical Research | Year: 2012

Alzheimer's disease (AD) diagnosis still depends on the triad of clinical, imaging and neuropsychological testing. The development of accurate, easy to use and inexpensive biological markers for AD is a long-standing aspiration for researchers and the medical community. Here we describe some of the recent advances in the field of biomarkers, both in cerebrospinal fluid (CSF) and in peripheral blood. © 2012 IMSS. Source

Carrasco-Gallardo C.,International Center for Biomedicine | Carrasco-Gallardo C.,University of Chile | Farias G.A.,International Center for Biomedicine | Fuentes P.,University of Chile | And 3 more authors.
Archives of Medical Research | Year: 2012

Alzheimer's disease (AD) is a brain disorder displaying a prevalence and impact in constant expansion. This expansive and epidemic behavior is concerning medical and public opinion while focusing efforts on its prevention and treatment. One important strategy to prevent this brain impairment is based on dietary changes and nutritional supplements, functional foods and nutraceuticals. In this review we discuss the potential contributions of shilajit and complex B vitamins to AD prevention. We analyze the status of biological studies and present data of a clinical trial developed in patients with mild AD. Studies suggest that shilajit and its active principle fulvic acid, as well as a formula of shilajit with B complex vitamins, emerge as novel nutraceutical with potential uses against this brain disorder. © 2012 IMSS. Source

Morales I.,International Center for Biomedicine | Farias G.,International Center for Biomedicine | MacCioni R.B.,International Center for Biomedicine
NeuroImmunoModulation | Year: 2010

Evidence has been cumulated on the role of microglia cells deregulation and alterations in their interaction patterns with brain neurons, in the pathway towards neurodegeneration in Alzheimer's disease (AD). After the failure of the amyloid hypothesis to explain AD pathogenesis, current hypotheses focus on tau self-polymerization into pathological oligomers and filaments as a major culprit for neurofibrillary degeneration. It is worth pointing out that formation of tau polymers is consistent with the clinical and neuropathological observations, and that tangles are pathognomonic of AD and related tau disorders. In this context, inflammatory processes play a major role in neuronal degeneration. On the basis of studies on microglia and neuronal cultures, together with experiments in animal models, and the clinical evidence, we postulated that a series of endogenous damage signals activate microglia cells, inducing NFκ-β with the consequent release of cytokine mediators such as TNF-α, IL-6 and IL-1β. An overexpression of these mediators may trigger signaling cascades in neurons leading to activation of protein kinases gsk3β, cdk5, abl kinases, along with inactivation of phosphatases such as PP1, with the resulting hyperphosphorylation and self-aggregation of tau protein into neurotoxic oligomeric species. © 2010 S. Karger AG, Basel. Source

Farias G.,University of Chile | Farias G.,International Center for Biomedicine | Farias G.,Cognitive Neurology and Dementia Unit | Perez P.,University of Chile | And 2 more authors.
Journal of Alzheimer's Disease | Year: 2012

Platelets are major reservoirs of circulating amyloid-β and amyloid-β protein precursor (AβPP) and have been postulated as a reliable source for biological markers of Alzheimer's disease (AD). We have recently demonstrated that tau is also present in platelets, and that there are differences in the electrophoretic patterns of platelet tau forms in AD subjects with respect to controls. Here, we demonstrate that modifications in platelet tau forms occur independently of age in a broad population of 104 neurologically healthy individuals. More interesting, a strong correlation of platelet markers with the degree of cognitive impairment was evidenced in a group of 47 AD patients in comparison with 19 cognitive healthy subjects. In our series, platelet tau forms ratio had a sensitivity of 75.7% and specificity of 73.7%, respectively. We also found that platelet tau displays a significantly higher correlation with the presence of AD than the analyses of platelet AβPP. © 2012 - IOS Press and the authors. All rights reserved. Source

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