About
28
Publications
7,924
Reads
How we measure 'reads'
A 'read' is counted each time someone views a publication summary (such as the title, abstract, and list of authors), clicks on a figure, or views or downloads the full-text. Learn more
819
Citations
Introduction
Laura Xicota currently works at the Gertrude H Sergievsky Center at Columbia University Medical Center. Laura does research in Neuroscience, working currently in Down syndrome and Alzheimer's disease. Her research focuses on genetics and biomarkers of disease.
Skills and Expertise
Additional affiliations
September 2017 - present
September 2011 - October 2016
October 2010 - June 2011
Publications
Publications (28)
Background:
One of the biggest challenge in Alzheimer's disease (AD) is to identify pathways and markers of disease prediction easily accessible, for prevention and treatment. Here we analysed blood samples from the INveStIGation of AlzHeimer's predicTors (INSIGHT-preAD) cohort of elderly asymptomatic individuals with and without brain amyloid loa...
Enlarged early endosomes have been visualized in Alzheimer’s disease (AD) and Down syndrome (DS) using conventional confocal microscopy at a resolution corresponding to endosomal size (hundreds of nm). In order to overtake the diffraction limit, we used super-resolution structured illumination microscopy (SR-SIM) and transmission electron microscop...
Pharmacotranscriptomics is a still very new field of research that has just begun to flourish and promises to enable target discovery, inform biomarker and evaluate drug efficacy beyond pharmacogenomics. The aim of this review is to provide a critical overview of the biological foundations of transcriptomics, methodological approaches to transcript...
Background and objectives
Brain amyloid deposition, a major risk factor for Alzheimer’s disease (AD), is currently estimated by measuring cerebrospinal fluid or plasma amyloid peptide levels, or by positron-emission tomography imaging. Assessing genetic risks relating to amyloid deposition before any accumulation has occurred would allow for earlie...
Morphological alterations of the endosomal compartment have been widely described in post-mortem brains from Alzheimer’s disease (AD) patients and subjects with Down syndrome (DS) who are at high risk for AD. Immunostaining with antibodies against endosomal markers such as Early Endosome Antigen 1 (EEA1) revealed increased size of EEA1-positive pun...
INTRODUCTION
This study aimed to investigate the influence of the overall Alzheimer's disease (AD) genetic architecture on Down syndrome (DS) status, cognitive measures, and cerebrospinal fluid (CSF) biomarkers.
METHODS
AD polygenic risk scores (PRS) were tested for association with DS‐related traits.
RESULTS
The AD risk PRS was associated with d...
To study mental illness and health, in the past researchers have often broken down their complexity into individual subsystems (e.g., genomics, transcriptomics, proteomics, clinical data) and explored the components independently. Technological advancements and decreasing costs of high throughput sequencing has led to an unprecedented increase in d...
Variation in the expression level and activity of genes involved in drug disposition and action in tissues of pharmacological importance have been increasingly investigated in patients treated with psychotropic drugs. Findings are promising, but reliable predictive biomarkers of response have yet to be identified. Here we conducted a PRISMA-complia...
Omics technologies offer great promises for improving our understanding of diseases. The integration and interpretation of such data pose major challenges, calling for adequate knowledge models. Disease maps provide curated knowledge about disorders' pathophysiology at the molecular level adapted to omics measurements. However, the expressiveness o...
Synaptic loss and neuronal cell death precede the cognitive symptoms of Alzheimer's disease by decades; therefore, it is vital to find preventive treatments that can act before they appear. The green tea flavanol epigallocatechin gallate (EGCG) has gained interest as a possible treatment after observational studies linked green tea consumption to l...
Background & Aims
Individuals with Down syndrome (DS) have higher rates of obesity. In the general population green tea extracts, and in particular epigallocatechin gallate (EGCG), have been studied for their antiobesogenic effects. The aim of this study is to elucidate the effect of EGCG on body weight in young DS adults and whether it could be r...
Cannabinoid CB1 receptors (CB1R) and serotonergic 2A receptors (5HT2AR) form heteromers in the brain of mice where they mediate the cognitive deficits produced by delta-9-tetrahydrocannabinol. However, it is still unknown whether the expression of this heterodimer is modulated by chronic cannabis use in humans. In this study, we investigated the ex...
Background:
MDMA has been shown to induce feelings of sociability, a positive emotional bias and enhanced empathy. While previous research has used only visual emotional stimuli, communication entails more than that single dimension and it is known that auditory information is also crucial in this process. In addition, it is, however, unclear what...
Objective:
Recent studies have underlined the effect of systemic inflammation on the pathophysiology of Alzheimer's disease. Neutrophils are key components of early innate immunity and contribute to uncontrolled systemic inflammation if not tightly regulated. The aim of our study was to fully characterize human circulating neutrophils at different...
MDMA exerts its main effects via the serotonergic system and the serotonin transporter. The gene coding for this transporter determines the expression rate of the transporter. Previously it was shown that healthy individuals with the short allelic variant ('s-group') of the 5-HTTLPR-polymorphism displayed more anxiety and negative mood, and had a l...
Down syndrome (DS) is an aneuploidy syndrome that is caused by trisomy for human chromosome 21 resulting in a characteristic cognitive and behavioral phenotype, which includes executive functioning and adaptive behavior difficulties possibly due to prefrontal cortex (PFC) deficits. DS also present a high risk for early onset of Alzheimer Disease-li...
Background:
Early cognitive intervention is the only routine therapeutic approach used for amelioration of intellectual deficits in individuals with Down's syndrome, but its effects are limited. We hypothesised that administration of a green tea extract containing epigallocatechin-3-gallate (EGCG) would improve the effects of non-pharmacological c...
Down syndrome (DS) is an intellectual disability (ID) disorder in which language and specifically, verbal fluency are strongly impaired domains; nearly all adults show neuropathology of Alzheimer’s disease (AD), including amyloid deposition by their fifth decade of life. In the general population, verbal fluency deficits are considered a strong AD...
Medical advances in the last decades have increased the average life expectancy, but also the incidence and prevalence of age-associated neurodegenerative diseases. Alzheimer disease (AD) is one of the most common neurodegenerative diseases and the most prevalent type of dementia. A plethora of different mechanisms contribute to AD, among which oxi...
Adherence to the Mediterranean Diet (MD) has been associated with a reduced incidence of neurodegenerative diseases and better cognitive performance. Virgin olive oil, the main source of lipids in the MD, is rich in minor phenolic components, particularly hydroxytyrosol (HT). HT potent antioxidant and anti-inflammatory actions have attracted resear...
Treatment with a sphingosine-1-phosphate analog inhibits airway remodeling
following repeated allergen exposure. Am J Physiol Lung Cell Mol
Physiol 302: L736–L745, 2012. First published January 27, 2012;
doi:10.1152/ajplung.00050.2011.—Sphingosine-1-phosphate (S1P) is
an immunomodulatory lipid mediator that plays an important role in
lymphocyte tra...
Questions
Questions (3)
I am working on sucrose separation of the vesicular compartments both in human cells and mouse brain samples. In order to validate the protocol, I am identifying the fraction where the different vesicular compartments end through Western Blot. I use a basic WB protocol with denaturating conditions (TGS 1X as running buffer, TGX 4-20% polyacrylamide precast gels, TG 1X + 20% EtOH as transfer buffer, TBS 1X 5% BSA 0.1% Tween 20 as blocking and for the primary overnight incubation, and TBS 1X 0.1% Tween for the secondary incubation).
I have been able to successfully detect Rab5, Rab7, and EEA1 on my usual conditions, with a clean and good signal. However, none of the potential lysosomal markers I have tried have worked. So far I have tried five different LAMP-1 Santa Cruz antibodies (even if LAMP1 can also be found on late endosomes), and one Cathepsin B, without success. Some people have told me that I might need to try a non-denaturing protocol to successfully detect LAMP-1, but they also told me that there were other things that needed to be changed and that they didn't have the protocol.
Does anyone have a good protocol to detect LAMP-1 or Cathepsin on WB? Antibody recommendations are also welcome!
Thanks!
Hi everyone,
in the lab we are interested in the endolysosomal pathway and we have tried several antibodies to do IF of Rab7, however those that we have tried either not work at all or have a staining that looks predominantly cytoplasmatic instead of vesicular.
Anyone has a favorite anti-Rab7 antibody? The cells are human, so if it happens to be human-specific better.
Thank you.
Hello,
I am currently working with human fibroblasts obtained through skin biopsy and I'm trying to transfect them. I have used the standard transfection protocol that has been successfully used on similar cells in the lab before (Lipofectamine 2000 + 0.5-1.5 µg DNA) and a protocol from another laboratory that uses higher concentrations of both lipofectamine and plasmid, that worked in their hands using this same cell line. However, I am having lots of trouble setting it up as I have either too much cell death or negligible transfection. I have tried several Lipofectamine/plasmid concentrations, cell densities, and surfaces (plastic and glass), but nothing seems to work too well. Does anyone have specific advice on what I could change to improve my transfection conditions?
Thanks in advance.
