Alexandra Botté

ORCID: 0000-0003-4631-8404
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Down syndrome and intellectual disability research
  • Cellular transport and secretion
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Lysosomal Storage Disorders Research
  • Inflammation biomarkers and pathways
  • Neurological Disease Mechanisms and Treatments
  • Healthcare Systems and Public Health
  • Retinopathy of Prematurity Studies
  • Immunodeficiency and Autoimmune Disorders
  • Neurotransmitter Receptor Influence on Behavior
  • Schizophrenia research and treatment
  • Bone Metabolism and Diseases
  • Respiratory Support and Mechanisms
  • Hemodynamic Monitoring and Therapy
  • Retinal Diseases and Treatments
  • Blood properties and coagulation
  • Retinal Imaging and Analysis
  • Calcium signaling and nucleotide metabolism
  • Central Venous Catheters and Hemodialysis
  • Eicosanoids and Hypertension Pharmacology
  • Pneumonia and Respiratory Infections
  • Lipid Membrane Structure and Behavior
  • Biomedical Research and Pathophysiology

University of Chicago
2016-2023

Pitié-Salpêtrière Hospital
2017-2023

Sorbonne Université
2017-2023

Institut du Cerveau
2019-2023

Assistance Publique – Hôpitaux de Paris
2020-2023

Inserm
2019-2021

Centre National de la Recherche Scientifique
2019-2021

Allen Institute for Brain Science
2021

Université d'été de Boulogne-sur-Mer
2017

Abstract Background Genome-wide association studies have identified BIN1 within the second most significant susceptibility locus in late-onset Alzheimer’s disease (AD). undergoes complex alternative splicing to generate multiple isoforms with diverse functions cellular processes including endocytosis and membrane remodeling. An increase expression AD an interaction between Tau been reported. However, disparate descriptions of localization brain previously reported literature lack clarity on...

10.1186/s13024-016-0124-1 article EN cc-by Molecular Neurodegeneration 2016-08-03

Abstract The current SARS-CoV-2 outbreak, which causes COVID-19, is particularly devastating for individuals with chronic medical conditions, in particular those Down Syndrome (DS) who often exhibit a higher prevalence of respiratory tract infections, immune dysregulation and potential complications. incidence Alzheimer’s disease (AD) much DS than the general population, possibly increasing further risk COVID-19 infection its Here we provide biological overview regard to specific...

10.1007/s12017-021-08651-5 article EN cc-by NeuroMolecular Medicine 2021-03-04

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 antibodies against markers such as Early Endosome Antigen 1 (EEA1) revealed increased size EEA1-positive puncta. In DS, peripheral cells blood mononuclear (PBMCs) fibroblasts, share similar phenotype even absence We previously found that PBMCs AD larger puncta,...

10.1038/s41398-023-02355-z article EN cc-by Translational Psychiatry 2023-02-14

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 overtake the diffraction limit, we used super-resolution structured illumination (SR-SIM) transmission electron microscopies (TEM) analyze compartment DS.By immunofluorescence microscopy, confirmed that volume Early Endosome Antigen 1 (EEA1)-positive puncta was 13-19% larger...

10.1186/s40478-020-00956-z article EN cc-by Acta Neuropathologica Communications 2020-06-24

Abstract Background Genome‐wide association studies (GWAS) have shown that single nucleotide polymorphisms (SNPs) within the membrane‐spanning 4‐domains subfamily A (MS4A) gene locus are linked with protection from Alzheimer’s Disease (AD) risk, delayed age‐at‐onset, and reduced expression of MS4A4A MS4A6A in myeloid cells. Recently, protective variants MS4A region been associated increased levels soluble triggering receptor expressed on cells 2 (sTREM2). Despite these associations,...

10.1002/alz.072144 article EN Alzheimer s & Dementia 2023-12-01

Abstract Background RIP Kinase 1 (RIPK1) is known to regulate necroptotic cell death in response pro‐inflammatory signaling cells where apoptotic has been compromised. Aberrant RIPK1 activation implicated several neurodegenerative disorders such as Alzheimer’s disease, Multiple Sclerosis, and Amyotrophic Lateral Sclerosis. Method To investigate the role of regulating microglial demyelination, we administered a highly selective CNS penetrant inhibitor C57Bl6 mice fed with cuprizone. We...

10.1002/alz.077538 article EN Alzheimer s & Dementia 2023-12-01

Trisomy of APP is responsible for extremely high incidence and early onset AD pathology in Down syndrome (DS) brains. However, other genes on human chr21 likely modulate the age onset, severity modality clinical picture, as DS individuals have later or absent AD, less intracerebral haemorrhage pathology, than euploid with familial caused by a duplication gene (dupAPP). Our aim to identify such modulator using cellular models. Neurons derived from isogenic hiPSCs we generated mosaic...

10.1016/j.jalz.2017.06.1380 article EN Alzheimer s & Dementia 2017-07-01
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