9 results match your criteria: "Mother and Teacher Pontifical Catholic University[Affiliation]"

With the COVID-19 pandemic, behavioural scientists aimed to illuminate reasons why people comply with (or not) large-scale cooperative activities. Here we investigated the motives that underlie support for COVID-19 preventive behaviours in a sample of 12,758 individuals from 34 countries. We hypothesized that the associations of empathic prosocial concern and fear of disease with support towards preventive COVID-19 behaviours would be moderated by trust in the government.

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Synonymous variants associated with Alzheimer disease in multiplex families.

Neurol Genet

August 2020

The Taub Institute for Research on Alzheimer's Disease and the Aging Brain (M.E.A., B.V., R.L., P.L.J., R.M., I.S.-M., C.R.); The Gertrude H. Sergievsky Center (M.T., D.R.-D., R.L., R.M., C.R.); Department of Neurology (P.L.J., R.M., C.R.); Department of Epidemiology (R.M., C.R.); Department of Psychiatry (R.M.), Columbia University, New York; Department of Pathology and Cell Biology (M.E.A., I.S.-M.), Columbia University, New York; Rush Alzheimer's Disease Center (D.A.B.); Department of Neurological Sciences (D.A.B.); Department of Pathology (D.A.B.), Rush University Medical Center, Chicago, IL; Center for Innovation in Brain Science , Departments of Pharmacology and Neurology , University of Arizona College of Medicine (M.T.), Tucson; Department of Medicine (R.L.), College of Physicians and Surgeons, Columbia University, New York, NY; School of Medicine (M.M.), Mother and Teacher Pontifical Catholic University, Santiago, Dominican Republic; and The Krembil Centre for Neuroinformatics (D.F.), Centre for Addiction and Mental Health, Toronto, Ontario, Canada.

Objective: Synonymous variants can lead to disease; nevertheless, the majority of sequencing studies conducted in Alzheimer disease (AD) only assessed coding variation.

Methods: To detect synonymous variants modulating AD risk, we conducted a whole-genome sequencing study on 67 Caribbean Hispanic (CH) families multiply affected by AD. Identified disease-associated variants were further assessed in an independent cohort of CHs, expression quantitative trait locus (eQTL) data, brain autopsy data, and functional experiments.

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To assess the effects of chronic alcoholism on the repair of bone defects associated with xenograft. Forty male rats were distributed in: control group (CG, = 20) and experimental group (EG, = 20), which received 25% ethanol ad libitum after a period of adaptation. After 90 days of liquid diet, the rats were submitted to 5.

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The incidence and prevalence of Alzheimer's disease (AD) dementia are higher among Caribbean Hispanics than among non-Hispanic Whites. The causes of this health disparity remain elusive, partially because of the relative limited capacity for biomedical research in the developing countries that comprise Caribbean Latin America. To begin to address this issue, we were awarded a Development Research Award from the US NIH and Fogarty International Center in order to establish the local capacity to integrate magnetic resonance imaging (MRI) into studies of cognitive aging and dementia in Dominican Republic, establish collaborations with Dominican investigators, and conduct a pilot study on the role of cerebrovascular markers in the clinical expression of AD.

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Objective: To identify rare causal variants underlying known loci that segregate with late-onset Alzheimer's disease (LOAD) in multiplex families.

Methods: We analyzed whole genome sequences (WGS) from 351 members of 67 Caribbean Hispanic (CH) families from Dominican Republic and New York multiply affected by LOAD. Members of 67 CH and additional 47 Caucasian families underwent WGS as a part of the Alzheimer's Disease Sequencing Project (ADSP).

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Objective: To determine whether the extent of overlap of the genetic architecture among the sporadic late-onset Alzheimer's Disease (sLOAD), familial late-onset AD (fLOAD), sporadic early-onset AD (sEOAD), and autosomal dominant early-onset AD (eADAD).

Methods: Polygenic risk scores (PRSs) were constructed using previously identified 21 genome-wide significant loci for LOAD risk.

Results: We found that there is an overlap in the genetic architecture among sEOAD, fLOAD, and sLOAD.

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Ultra-rare mutations in segregate in Caribbean Hispanic families with Alzheimer disease.

Neurol Genet

October 2017

Taub Institute for Research on Alzheimer's Disease and the Aging Brain (B.N.V., G.T., R. Lefort, P.L.D.J., S.B., D.R.-D., J.H.L., R.C., R. Lantigua, R.M.); Gertrude H. Sergievsky Center (B.N.V., G.T., S.B., D.R.-D., J.H.L., R.C., R.M.); Department of Neurology (P.L.D.J., S.B., R.M.), Department of Psychiatry (R.M.), Department of Systems Biology (B.N.V.), Department of Medicine (R. Lantigua), and Department of Pathology and Cell Biology (R. Lefort, P.L.N.), College of Physicians and Surgeons, Columbia University, New York Presbyterian Hospital; Department of Epidemiology (J.H.L., R.M.), School of Public Health, Columbia University, New York; Tanz Centre for Research in Neurodegenerative Diseases (E.R., P.S.G.-H.) and Department of Medicine (E.R., P.S.G.-H.), University of Toronto, Krembil Discovery Tower, ON, Canada; Department of Clinical Neurosciences (P.S.G.-H.), Cambridge Institute for Medical Research, University of Cambridge, UK; Rush Alzheimer's Disease Center (L.Y., D.A.B.), Rush University Medical Center, Chicago, IL; Program in Medical and Population Genetics (P.L.D.J.), Broad Institute, Cambridge, MA; and School of Medicine (M.M.), Mother and Teacher Pontifical Catholic University, Santiago, Dominican Republic.

Objective: To identify rare coding variants segregating with late-onset Alzheimer disease (LOAD) in Caribbean Hispanic families.

Methods: Whole-exome sequencing (WES) was completed in 110 individuals from 31 Caribbean Hispanic families without homozygous carriers. Rare coding mutations segregating in families were subsequently genotyped in additional families and in an independent cohort of Caribbean Hispanic patients and controls.

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Polygenic risk scores in familial Alzheimer disease.

Neurology

March 2017

From the Taub Institute for Research on Alzheimer's Disease and the Aging Brain (G.T., J.M., R.O., N.S., Y.S., R.M.), Gertrude H. Sergievsky Center (G.T., J.M., N.S., Y.S., R.M.), and Department of Neurology (G.T., J.M., R.O., N.S., Y.S.), Columbia University College of Physicians and Surgeons, New York; New York Presbyterian Hospital (G.T., J.M., R.O., N.S., Y.S.), NY; Departments of Neurology and Medicine (T.D.B., D.T.), University of Washington, Seattle; Rush Alzheimer's Disease Center (D.A.B.), Rush University Medical Center, Chicago, IL; Department of Neurology (B.F.B.), Mayo Clinic, Rochester, MN; Hope Center for Neurological Disorders (C.C.), Washington University, St Louis, MO; Department of Medical and Molecular Genetics (K.F., T.M.F.), Indiana University; Department of Neurology (M.F.), Indiana University Center for Alzheimer's Disease and Related Disorders, Indianapolis; Department of Neuroscience (A.M.G., S.B.), Mount Sinai School of Medicine, New York, NY; Department of Neurology (N.R.G.-R.), Mayo Clinic, Jacksonville, FL; School of Medicine (M.M., R.M.), Mother and Teacher Pontifical Catholic University, Santiago, Dominican Republic; Department of Medicine (R.L.) and Department of Epidemiology, Mailman School of Public Health (R.O., N.S.), Columbia University, New York; Division of Epidemiology (R.O.), New York State Psychiatric Institute, New York; Department of Neurology and Neurotherapeutics (R.R.), The University of Texas Southwestern Medical Center, Dallas; Department of Health Sciences Research (D.J.S.), Mayo Clinic, Rochester, MN; and Department of Psychiatry, Neurology and Epidemiology (R.A.S.), University of Pittsburgh, PA.

Objective: To investigate the association between a genetic risk score (GRS) and familial late-onset Alzheimer disease (LOAD) and its predictive value in families multiply affected by the disease.

Methods: Using data from the National Institute on Aging Genetics Initiative for Late-Onset Alzheimer Disease (National Institute on Aging-Late-Onset Alzheimer's Disease Family Study), mixed regression models tested the association of familial LOAD with a GRS based on single nucleotide polymorphisms (SNPs) previously associated with LOAD. We modeled associations using unweighted and weighted scores with estimates derived from the literature.

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Objective: To detect rare coding variants underlying loci detected by genome-wide association studies (GWAS) of late onset Alzheimer disease (LOAD).

Methods: We conducted targeted sequencing of ABCA7, BIN1, CD2AP, CLU, CR1, EPHA1, MS4A4A/MS4A6A, and PICALM in 3 independent LOAD cohorts: 176 patients from 124 Caribbean Hispanics families, 120 patients and 33 unaffected individuals from the 129 National Institute on Aging LOAD Family Study; and 263 unrelated Canadian individuals of European ancestry (210 sporadic patients and 53 controls). Rare coding variants found in at least 2 data sets were genotyped in independent groups of ancestry-matched controls.

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