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1. Determinación de anticuerpos anti-β2glicoproteína I en pacientes con síndrome antifosfolípido Anti- β2 glycoprotein antibodies in patients with antiphospholipid syndrome

Author

Oscar Uribe Uribe, Jorge Humberto Botero Garcés, Ruth Beatriz Peña Arboleda, Juan Carlos Quintana Zapata, María Leonor Alvarez Peláez, Gloria Patricia García Ospina, and Angela Patricia Cadavid Jaramillo

Subjects
anticuerpos anti-β2gpi, anticuerpos anticardiolipina, pérdida recurrente del embarazo, sindrome antifosfolípido, trombosis, anti- β 2glycoprotein i antibodies, anticardiolipin antibodies, antiphospholipid syndrome, recurrent pregnancy loss, thrombosis, Medicine, Medicine (General), R5-920
Abstract

EL objetivo de este estudio fue comparar la presencia de anticuerpos anti-β2glicoproteína I (anti- β2GPI) con las pruebas convencionales de laboratorio de anticuerpos anticardiolipina (aCL) y anticoagulante lúpico, y con las manifestaciones clínicas del síndrome antifosfolípido (SAF). Se incluyeron en el estudio 80 mujeres con SAF; 35 de ellas de la consulta de Reumatología y las otras 45 con historia de aborto recurrente espontáneo (ARE); 5 mujeres de la consulta de Reumatología sin SAF, 27 mujeres con ARE, sin SAF y un grupo control de 20 mujeres sanas en edad reproductiva. Se investigaron la presencia de anticuerpos IgG e IgM anticardiolipina (aCL) e IgG anti- β2GPI por la técnica de ELISA, y el anticoagulante lúpico por la determinación del tiempo parcial de tromboplastina activado. Adicionalmente, se registraron las manifestaciones clínicas asociadas al SAF. De las pacientes con SAF, 25.7% del grupo de Reumatología (9/35) y 4.4% de las pacientes con ARE (2/45) fueron positivas para anticuerpos anti-β2GPI, mientras que ninguna de las mujeres sin SAF, ni de las mujeres del grupo control, fue positiva. La asociación entre la presencia de anti- β2GPI y los anticuerpos IgG e IgM aCL mostró una diferencia significativa en los títulos de 3+ (altamente positivos) en contraste con los individuos negativos para anti- β2GPI. La positividad del anticoagulante lúpico también se correlacionó con la presencia de anticuerpos anti- β2GPI. No hubo diferencia significativa entre las diversas manifestaciones clínicas del SAF y la presencia de dichos anticuerpos. En conclusión, la determinación de anticuerpos anti- β2GPI tiene una alta especificidad en pacientes con SAF pero no se asoció con ninguna manifestación clínica en particular. The objective of this study was to compare the presence of anti-β2glycoprotein (anti- β2GPI) antibodies with the conventional laboratory tests of anticardiolipin antibodies (aCL) and lupus anticoagulant and with the clinical manifestations of the Antiphospholipid Syndrome (APS). In this study 80 women with APS (35 from the Rheumatology Service and 45 with a history of recurrent spontaneous abortion, RSA) were included, as well as 5 women with rheumatic diseases but no APS, 27 RSA-women without APS and 20 healthy women in their reproductive age. The presence of IgG and IgM anticardiolipin antibodies (aCL), anti- β2GPI antibodies by ELISA method and lupus anticoagulant by the test of activated partial thromboplastin time was investigated. Additionally the clinical manifestations associated to APS were registered. In the group of women with APS, 25.7% (9/35) of those with rheumatic diseases and 4.4% /2/45) of the ones with RSA were positive for anti- β2GPI while none of the women without APS or the controls had such positive reaction. There was a significant association at titers of 3+ (highly positive) between the presence of anti- β2GPI antibodies and IgG and IgM aCL in contrast to anti- β2GPI-negative individu als. The positivity of lupus anticoagulant also correlated with the presence of anti- β2GPI antibodies. There was no significant correlation between any specific clinical manifestation and the presence of anti- β2GPI antibodies. In conclusion, the determination of anti- β2GPI antibodies was highly specific in patients with APS but did not associate with any clinical manifestation of the syndrome.

Published
2004

2. El β-Amiloide: modulador de inflamación en la enfermedad de Alzheimer

Author

Marlene Jiménez del Río, Carlos Vélez Pardo, and Gloria Patricia García Ospina

Subjects
Alzheimer, β-Amiloide, Medicine, Medicine (General), R5-920
Abstract

El depósito del fragmento péptido de βamiloide [1-42] (βA[1-42]) constituye una de las principales características neuropatológicas y el principal componente de las placas seniles en la enfermedad de Alzheimer (EA). Este pèptico se deriva de la proteína precursora de amiloide (PPA) y es un factor desencadenante de una respuesta inflamatoria crónica en los cerebros de los individuos afectados. Esta respuesta, modulada por el βA, se caracteriza por la inducción de una cascada de eventos moleculares que incluye la activación de la microglia y la astroglia, la activación del complemento por las vías clásica y alterna, la expresión y secreción de citoquinas, interleuquinas y proteínas de fase aguda y la secreción de βA. Todos estos factores actúan en concierto, generando un conjunto de reacciones cíclicas con efectos deletéreos para las neuronas y la glia en la EA. Esta revisión científica reúne las evidencias experimentales que implican al βA como péptido modulador en el proceso inflamatorio. Adicionalmente, se presenta un modelo hipotético que explica el papel que juega el βA como agente generador del proceso de inflamación crónica en la enfermedad de Alzheimer. Esta información podría ser un aporte a una mejor comprensión de los eventos moleculares proinflamatorios y antiinflamatorios que contribuyen a la evolución de la enfermedad de Alzheimer y a un mayor conocimiento en el diseño de posibles estrategias terapéuticas antiinflamatorias que ayudarían a retardar la progresión y aparición de este desorden neurológico devastador.

Published
2001

3. The INECO Frontal Screening for the Evaluation of Executive Dysfunction in Cerebral Small Vessel Disease: Evidence from Quantitative MRI in a CADASIL Cohort from Colombia

Author

Dorothee Schoemaker, Carolina Ospina, Heirangi Torrico-Teave, Gloria Patricia García Ospina, Yakeel T. Quiroz, Anand Viswanathan, Yesica Zuluaga, Francisco Lopera, Joseph F. Arboleda-Velasquez, Markus Shrimer, and Lina Velilla

Subjects
Adult, Male, medicine.medical_specialty, CADASIL, Context (language use), Colombia, Neuropsychological Tests, Asymptomatic, 050105 experimental psychology, Cohort Studies, Leukoencephalopathy, Executive Function, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Humans, Cognitive Dysfunction, 0501 psychology and cognitive sciences, medicine.diagnostic_test, Receiver operating characteristic, business.industry, General Neuroscience, 05 social sciences, Neuropsychology, Magnetic resonance imaging, Middle Aged, medicine.disease, Magnetic Resonance Imaging, Psychiatry and Mental health, Clinical Psychology, Cross-Sectional Studies, Cerebral Small Vessel Diseases, Cardiology, Female, Neurology (clinical), medicine.symptom, Cognition Disorders, business, 030217 neurology & neurosurgery, Executive dysfunction
Abstract

Objectives:Executive dysfunction is a predominant cognitive symptom in cerebral small vessel disease (SVD). The Institute of Cognitive Neurology Frontal Screening (IFS) is a well-validated screening tool allowing the rapid assessment of multiple components of executive function in Spanish-speaking individuals. In this study, we examined performance on the IFS in subjects with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), an inherited condition leading to the early onset of SVD. We further explored associations between performance on the IFS and magnetic resonance imaging (MRI) markers of SVD.Methods:We recruited 24 asymptomatic CADASIL subjects and 23 noncarriers from Colombia. All subjects underwent a research MRI and a neuropsychological evaluation, including the IFS. Structural MRI markers of SVD were quantified in each subject, together with an SVD Sum Score representing the overall burden of cerebrovascular alterations. General linear model, correlation, and receiver operating characteristic curve analyses were used to explore group differences on the IFS and relationships with MRI markers of SVD.Results:CADASIL subjects had a significantly reduced performance on the IFS Total Score. Performance on the IFS correlated with all quantified markers of SVD, except for brain atrophy and perivascular spaces enlargement. Finally, while the IFS Total Score was not able to accurately discriminate between carriers and noncarriers, it showed adequate sensitivity and specificity in detecting the presence of multiple MRI markers of SVD.Conclusions:These results suggest that the IFS may be a useful screening tool to assess executive function and disease severity in the context of SVD.

Published
2020
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4. O2–03–05: Alzheimer's Prevention Initiative Colombia registry in the PSEN1 E280A mutation kindred

Author

Pierre N. Tariot, Sonia Moreno, Liliana Lopez, Claudia Muñoz, Eric M. Reiman, William Cho, Francisco Lopera, Victoria Tirado, Gloria Patricia García Ospina, Shehnaaz Suliman, Natalia Acosta, Carole Ho, Jessica B. Langbaum, and Margarita Giraldo

Subjects
Genetics, Gerontology, Epidemiology, business.industry, Health Policy, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Mutation (genetic algorithm), PSEN1, Medicine, Neurology (clinical), Geriatrics and Gerontology, business
Published
2013
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5. Abeta[25-35] peptide and iron promote apoptosis in lymphocytes by an oxidative stress mechanism: involvement of H2O2, caspase-3, NF-kappaB, p53 and c-Jun

Author

Carlos Velez-Pardo, Marlene Jimenez Del Rio, and Gloria Patricia García Ospina

Subjects
Adult, Male, Programmed cell death, Iron, Blotting, Western, Caspase 3, Apoptosis, Electrophoretic Mobility Shift Assay, In Vitro Techniques, Toxicology, medicine.disease_cause, chemistry.chemical_compound, Genes, jun, medicine, Humans, Senile plaques, Lymphocytes, RNA, Messenger, Caspase, Amyloid beta-Peptides, biology, Cell Death, General Neuroscience, c-jun, NF-kappa B, NF-κB, Hydrogen Peroxide, Genes, p53, Molecular biology, Immunohistochemistry, Peptide Fragments, Oxidative Stress, chemistry, Caspases, Immunology, biology.protein, Reactive Oxygen Species, Oxidative stress
Abstract

The Aβ deposition in the neuritic plaques is one of the major neuropathological hallmarks of the Alzheimer disease (AD). Studies in vitro have demonstrated that the Aβ 25–35 fragment, which contains the cytotoxic functional sequence of the amyloid peptide, induces neurotoxicity and cell death by apoptosis. Despite intense investigations, a complete picture of the precise molecular cascade leading to cell death in a single cellular model is still lacking. In this study, we provide evidence that Aβ 25–35 induce apoptosis either alone or in presence of iron in peripheral blood lymphocytes cells (PBL) in a concentration-dependent fashion by an oxidative stress mechanism involving: (1) the production of hydrogen peroxide (H 2 O 2 ), reflected by rhodamine-positive fluorescent cells, (2) activation and/or translocation of NF-κB, p53 and c-Jun transcription factors showed by immunocytochemical diaminobenzidine positive nuclei, (3) activation of NF-κB complex by electrophoretic mobility shift assay/immuno-blotting/and ammonium pyrrolidinedithiocarbamate (PDTC) inhibition, (4) caspase-3 activation, reflected by caspase Ac-DEVD-cho inhibition, (5) mRNA synthesis de novo according to actinomycin D cell death inhibition. These results are consistent with the notion that the Aβ 25–35 /H 2 O 2 generation precede the apoptotic process and that once H 2 O 2 is generated, it is able to trigger a specific cell death signalisation. Thus, taken together these results, we present a well-ordered cascade of the major molecular events leading PBL to apoptosis. These results may contribute to explain the importance of Aβ alone or in the presence of redox-available iron in association with Aβ plaques (and neurofibrillary tangles) in AD brains and the significant role played by H 2 O 2 as a second messenger of death signal in some degenerative diseases linked to oxidative stress stimuli.

Published
2002

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