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Prion disease and Alzheimer's disease: pathogenic overlap

100%
Castellani R. J., Perry G., Smith M. A.
Acta Neurobiologiae Experimentalis
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2004
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vol. 64
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issue 1
11-17
EN
Prion diseases are widely recognized for their transmissibility, and it is this feature that has been studied most extensively. In recent years, public health concerns over the transmission of animal forms of prion disease, such as bovine spongiform encephalopathy and chronic wasting disease, to humans has only augmented the notion that prion diseases are primarily infectious. Yet within the spectrum of human prion diseases, often overlooked is the fact that the overwhelming majority of cases are age-dependent sporadic, or inherited processes. Closer examination of the pathophysiological processes involved in prion disease further indicates a neurodegenerative, rather than infectious disease. Indeed, the age requirement, the numerous kindreds carrying point mutations in an amyloidogenic protein, the copper binding properties of the amyloidogenic protein, the evidence of free radical damage, the presence of polymorphisms that influence disease susceptibility, the formation of amyloid plaques, and in some cases the presence of neurofibrillary pathology, are features common to both prion disease and Alzheimer's disease. Therefore, while transmissibility will continue to be a major subject of prion disease research, we suspect that further characterization of its pathophysiological mechanisms will only substantiate the notion that prion disease is fundamentally a neurodegenerative process.
2
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Tau phosphorylation and assembly

100%
Gomez-Ramos A., Smith M. A., Perry G., Avila J.
Acta Neurobiologiae Experimentalis
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2004
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vol. 64
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issue 1
33-39
EN
Neurofibrillary tangles, one of the aberrant structures found in the brain of Alzheimer's disease patients are mainly composed of tau in hyperphosphorylated form.Thus, a possible relation between phosphorylation and assembly of tau proteins has been analysed. By doing in vitro studies we have observed that in certain conditions, where compounds from oxidative stress are present, the capacity of tau for self assembly increases upon phosphorylation.
3
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Sources and mechanisms of cytoplasmic oxidative damage in Alzheimer's disease

88%
Marlatt M., Lee H., Perry G., Smith M. A., Zhu X.
Acta Neurobiologiae Experimentalis
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2004
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vol. 64
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issue 1
81-87
EN
While evidence supports a pathogenic and proximal role for oxidative stress in Alzheimer's disease, the causes and consequences of reactive oxygen species that promote oxidative damage have not been directly demonstrated. Co-incident with the reduced energy metabolism during the development of the disease, some of the key mitochondrial enzymes have shown deficient activity in AD neurons, which may lead to increased ROS production. However, we found that oxidative damage occurs primarily within the cytoplasm rather than in mitochondria. Given that SOD activity is increased in AD mitochondria and that metal ions such as iron and copper are enriched in susceptible neurons, we hypothesize that mitochondria, as a source, provide hydrogen peroxide, which, as an intermediate, once in the cytoplasm, will be converted into highly reactive hydroxyl radicals through Fenton reaction in the presence of metal ion and cause damage in cytoplasm.
4
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Gonadotropins and Alzheimer's disease: the link between estrogen replacement therapy and neuroprotection

76%
Webber K. M., Bowen R., Casadesus G., Perry G., Atwood C. S., Smith M. A.
Acta Neurobiologiae Experimentalis
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2004
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vol. 64
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issue 1
113-118
EN
The search for a definitive gender bias in Alzheimer's disease has resulted in a multitude of epidemiological findings that point to a higher prevalence and incidence of Alzheimer's disease in women. Due to this reported predisposition of women to Alzheimer's disease, the sex steroid estrogen has become the primary focus of research in this field, however, inconclusive data regarding estrogen replacement therapy has lead some researchers to further investigate the role of the other hormones of the hypothalamic-pituitary-gonadal (HPG) axis that have been, for the most, part overlooked. The hormones of the HPG axis, such as the gonadotropin, (luteinizing hormone and follicle-stimulating hormone), are involved in regulating reproductive function via a complex feedback loop. We propose that it is in fact the increase in gonadotropin concentrations and not the decrease in steroid hormone (e.g., estrogen) production following menopause/andropause that results in an increased risk of Alzheimer's disease. Furthermore, when the role of gonadotropins is taken into account, the data obtained from recent epidemiological studies and randomized trials suggesting the ineffectiveness estrogen may indeed be misinterpreted. In this review, we examine how hormones of the hypothalamic-pituitary-gonadal axis, in particular the gonadotropins, play a central and determining role in modulating the susceptibility to and progression of Alzheimer's disease. Based on this, we suggest that therapeutic interventions targeted at gonadotropins could both prevent disease in those patients currently asymptomatic or halt, and even reverse, disease in those currently afflicted.
5
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The role of metabotropic glutamate receptors in Alzheimer's disease

64%
Lee H., Zhu X., O'Neill M. J., Webber K., Casadesus G., Marlatt M., Raina A. K., Perry G., Smith M. A.
Acta Neurobiologiae Experimentalis
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2004
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vol. 64
|
issue 1
89-98
EN
While glutamatergic transmission is severely altered by early degeneration of cortico-cortical connections and hippocampal projections in Alzheimer's disease (AD), the role of glutamate receptors in the pathogenesis of AD is not yet defined clearly. Nonetheless, as reviewed here, the topographical distribution of different types of receptors likely contributes to the regional selective nature of neuronal degeneration. In particular, metabotropic glutamate receptors (mGluR) may contribute the pathogenesis of many neurological conditions and also regulate neuronal vulnerability against cytotoxic stress. Thus, we here discuss the possible role of mGluR in the pathogenesis of AD based on the results from other neurodegenerative diseases that may give us clues to solve the mysterious selective neurodegeneration evident in AD.
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