Browsing by Author "Von Bernhardi Montgomery, Rommy Edth B."

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    c-Abl tyrosine kinase modulates tau pathology and Cdk5 phosphorylation in AD transgenic mice
    (2011) Cancino Lobos, Gonzalo; Pérez De Arce Guzmán, Karen Andrea; Castro Uribe, Paula Andrea; Toledo Maldonado, Enrique Daniel; Von Bernhardi Montgomery, Rommy Edth B.; Álvarez Rojas, Alejandra Beatriz
    The c-Abl tyrosine kinase is an important link in signal transduction pathways that promote cytoskeletal rearrangement and apoptotic signalling. We have previously shown that amyloid-beta-peptide (A beta) activates c-Abl. Herein we show that c-Abl participates in A beta-induced tau phosphorylation through Cdk5 activation. We found that intraperitoneal administration of STI571, a specific inhibitor for c-Abl kinase, decreased tau phosphorylation in the APPswe/PSEN1 Delta E9 transgenic mouse brain. In addition, when neurons were treated with A beta we observed: (i) an increase in active c-Abl and tau phosphorylation, (ii) the prevention of tau phosphorylation by STI571 and (iii) the inhibition of c-Abl expression by shRNA, as well as the expression of a c-Abl kinase death mutant, decreased AT8 and PHF1 signals. Furthermore, the increase of c-Abl was associated with Tyr15 phosphorylation of Cdk5 and its association with c-Abl. Brains from APPswe/PSEN1 Delta E9 mice showed higher levels of c-Abl and phospho-Cdk5 than wild-type mice. Moreover, STI571 treatment decreased the phospho-Cdk5 levels. Together, the evidence suggests that activation of c-Abl by A beta promotes tau phosphorylation through Tyr15 phosphorylation-mediated Cdk5 activation. (C) 2009 Elsevier Inc. All rights reserved.
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    Clinical research in Chile: do not block the way of inquiry
    (2020) Valera, Luca; Ramos Vergara, Paulina Cecilia; Barrientos Zamorano, Marcelo; Altermatt Couratier, Fernando René; Ruiz Poblete, Sergio Marcelo; Von Bernhardi Montgomery, Rommy Edth B.; Cuello Fredes, Mauricio Arturo
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    El síndrome metabólico: de factor agravante a principal factor de riesgo patogénico en diversas enfermedades crónicas
    (2010) Von Bernhardi Montgomery, Rommy Edth B.; Zanlungo Matsuhiro, Silvana; Arrese Jiménez, Marco Antonio; Arteaga Llona, Antonio Alberto; Rigotti Rivera, Attilio Gianpietro
    In recent years, a rapidly increasing number of studies have focused on the association between metabolic syndrome and several chronic diseases. However, it is difficult to determine a well defined pathogenic relationship, due to the etiological heterogeneity and comorbidities of these diseases. Research efforts are aiming to identify the convergent biological mechanisms that mediate the effects of hyperinsulinemia, hyperglycemia, dyslipidemia, and hypertension. All these conditions define the metabolic syndrome, that increases the risk for several diseases. The knowledge of these biological mechanisms associated with this syndrome will elucidate the pathogenic association between a variety of chronic diseases, including its pathogenic link with cardiovascular diseases and the most common forms of dementia. The development of new therapeutic and preventive strategies for these diseases will be a corollary of this research.
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    Microglia Function in the Normal Brain
    (2016) Heredia, María Florencia; Muñoz Reyes, Paola Cecilia; Salgado Cortés, Nicole Andrea; Von Bernhardi Montgomery, Rommy Edth B.
    The activation of microglia has been recognized for over a century by their morphological changes. Long slender microglia acquire a short sturdy ramified shape when activated. During the past 20 years, microglia have been accepted as an essential cellular component for understanding the pathogenic mechanism of many brain diseases, including neurodegenerative diseases. More recently, functional studies and imaging in mouse models indicate that microglia are active in the healthy central nervous system. It has become evident that microglia release several signal molecules that play key roles in the crosstalk among brain cells, i.e., astrocytes and oligodendrocytes with neurons, as well as with regulatory immune cells. Recent studies also reveal the heterogeneous nature of microglia diverse functions depending on development, previous exposure to stimulation events, brain region of residence, or pathological state. Subjects to approach by future research are still the unresolved questions regarding the conditions and mechanisms that render microglia protective, capable of preventing or reducing damage, or deleterious, capable of inducing or facilitating the progression of neuropathological diseases. This novel knowledge will certainly change our view on microglia as therapeutic target, shifting our goal from their general silencing to the generation of treatments able to change their activation pattern.
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    The Challenge by Multiple Environmental and Biological Factors Induce Inflammation in Aging: Their Role in the Promotion of Chronic Disease
    (2020) Bachmann Barron, María Consuelo; Bellalta Bremer, Sofia Paz; Basoalto Escobar, Roque Ignacio; Gómez Valenzuela, Fernán Daniel; Jalil Contreras, Yorschua Frederick; Lepez Rivera, Macarena Paz; Matamoros, José Anibal; Von Bernhardi Montgomery, Rommy Edth B.
    The aging process is driven by multiple mechanisms that lead to changes in energy production, oxidative stress, homeostatic dysregulation and eventually to loss of functionality and increased disease susceptibility. Most aged individuals develop chronic low-grade inflammation, which is an important risk factor for morbidity, physical and cognitive impairment, frailty, and death. At any age, chronic inflammatory diseases are major causes of morbimortality, affecting up to 5-8% of the population of industrialized countries. Several environmental factors can play an important role for modifying the inflammatory state. Genetics accounts for only a small fraction of chronic-inflammatory diseases, whereas environmental factors appear to participate, either with a causative or a promotional role in 50% to 75% of patients. Several of those changes depend on epigenetic changes that will further modify the individual response to additional stimuli. The interaction between inflammation and the environment offers important insights on aging and health. These conditions, often depending on the individual's sex, appear to lead to decreased longevity and physical and cognitive decline. In addition to biological factors, the environment is also involved in the generation of psychological and social context leading to stress. Poor psychological environments and other sources of stress also result in increased inflammation. However, the mechanisms underlying the role of environmental and psychosocial factors and nutrition on the regulation of inflammation, and how the response elicited for those factors interact among them, are poorly understood. Whereas certain deleterious environmental factors result in the generation of oxidative stress driven by an increased production of reactive oxygen and nitrogen species, endoplasmic reticulum stress, and inflammation, other factors, including nutrition (polyunsaturated fatty acids) and behavioral factors (exercise) confer protection against inflammation, oxidative and endoplasmic reticulum stress, and thus ameliorate their deleterious effect. Here, we discuss processes and mechanisms of inflammation associated with environmental factors and behavior, their links to sex and gender, and their overall impact on aging.