Agnes Paulus

ORCID: 0009-0005-2587-3400
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Alzheimer's disease research and treatments
  • Tryptophan and brain disorders
  • Inflammation biomarkers and pathways
  • Galectins and Cancer Biology
  • Spectroscopy Techniques in Biomedical and Chemical Research
  • Advanced Fluorescence Microscopy Techniques
  • Stress Responses and Cortisol
  • Computational Drug Discovery Methods
  • Cholinesterase and Neurodegenerative Diseases
  • thermodynamics and calorimetric analyses
  • Quantum Dots Synthesis And Properties
  • Macrophage Migration Inhibitory Factor
  • Apelin-related biomedical research
  • School Health and Nursing Education
  • GDF15 and Related Biomarkers
  • Near-Field Optical Microscopy
  • Dutch Social and Cultural Studies

Lund University
2017-2023

UPMC Center for High Value Health Care
2022

Alzheimer's disease (AD) is a progressive neurodegenerative in which the formation of extracellular aggregates amyloid beta (Aβ) peptide, fibrillary tangles intraneuronal tau and microglial activation are major pathological hallmarks. One key molecules involved galectin-3 (gal3), we demonstrate here for first time role gal3 AD pathology. Gal3 was highly upregulated brains patients 5xFAD (familial disease) mice found specifically expressed microglia associated with Aβ plaques....

10.1007/s00401-019-02013-z article EN cc-by Acta Neuropathologica 2019-04-20

Alzheimer's disease (AD) is the most common form of dementia characterized by formation amyloid plaques (Aβ). Over last decade, important role innate immune system for development has been established. Chronic activation microglial cells creates a proinflammatory environment, which believed to be central as well its progression. We used AD mouse model 5xFAD investigate if inflammatory alterations are present in before plaque deposition. applied mass spectrometry and bioinformation analysis...

10.1038/s41598-018-19699-y article EN cc-by Scientific Reports 2018-01-18

Abstract Galectin-3 (Gal-3) is a beta-galactosidase binding protein involved in microglial activation the central nervous system (CNS). We previously demonstrated crucial deleterious role of Gal-3 Alzheimer’s disease (AD). Under AD conditions, primarily expressed by cells clustered around Aβ plaques both human and mouse brain, knocking out reduces pathology AD-model mice. To further unravel importance Gal-3-associated inflammation AD, we aimed to investigate inflammatory response continuum....

10.1007/s00401-022-02469-6 article EN cc-by Acta Neuropathologica 2022-07-27

Alzheimer’s disease (AD) accounts for about 70% of neurodegenerative diseases and is a cause cognitive decline death one-third seniors. AD currently underdiagnosed, it cannot be effectively prevented. Aggregation amyloid-β (Aβ) proteins has been linked to the development AD, established that, under pathological conditions, Aβ undergo structural changes form β-sheet structures that are considered neurotoxic. Numerous intensive in vitro studies have provided detailed information amyloid...

10.3390/cells10102559 article EN cc-by Cells 2021-09-27

Abstract Alzheimer’s disease (AD) is the most common cause of dementia, costing about 1% global economy. Failures clinical trials targeting amyloid-β protein (Aβ), a key trigger AD, have been explained by drug inefficiency regardless mechanisms amyloid neurotoxicity, which are very difficult to address available technologies. Here, we combine two imaging modalities that stand at opposite ends electromagnetic spectrum, and therefore, can be used as complementary tools assess structural...

10.1038/s41377-021-00590-x article EN cc-by Light Science & Applications 2021-07-22

Galectin-3 (Gal3) is a regulator of microglial activation implicated in Alzheimer's disease (AD). However, Gal3 role modulating phenotype towards amyloid-beta (Aβ) remains poorly understood. We demonstrate that affects several functions and binds Aβ fibrils with high affinity, stabilizing aggregation intermediates alter fibril kinetics morphology. Furthermore, deletion the direct relationship between microglia Aβ, reducing its uptake increasing compaction. AlphaFold modeling predicts...

10.1101/2025.03.17.643790 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2025-03-17

Early life adversities during childhood (such as maltreatment, abuse, neglect, or parental deprivation) may increase the vulnerability to cognitive disturbances and emotional disorders in both, adolescence adulthood. Maternal separation (MS) is a widely used model study stress-related changes brain behavior rodents. In this study, we investigated effect of MS (postnatal day 2–14, 3 ​h/day) female male adolescent mice. Specifically, evaluated (i) spatial working memory, anxiety...

10.1016/j.bbih.2020.100142 article EN cc-by Brain Behavior & Immunity - Health 2020-09-19

The risk of developing Alzheimer's disease (AD) is modulated by genetic and environmental factors. Early-life stress (ELS) exposure during critical periods brain development can impact later function health, including increasing the AD. Microglial dysfunction neuroinflammation have been implicated as playing a role in AD pathology may be ELS. To complicate matters further, sex-specific effects noted response to ELS incidence progression AD.Here, we subjected male female mice with either wild...

10.1186/s12974-022-02515-w article EN cc-by Journal of Neuroinflammation 2022-06-15

Light microscopy has been a favorite tool of biological studies for almost century, recently producing detailed images with exquisite molecular specificity achieving spatial resolution at nanoscale. However, light is insufficient to provide chemical information as standalone technique. An increasing amount evidence demonstrates that optical photothermal infrared microspectroscopy (O-PTIR) valuable imaging can extract locate structures submicron resolution. To further investigate the...

10.1016/j.nano.2022.102563 article EN cc-by-nc-nd Nanomedicine Nanotechnology Biology and Medicine 2022-04-30

Alzheimer’s disease affects millions of lives worldwide. This terminal is characterized by the formation amyloid aggregates, so-called oligomers. These oligomers are composed β-sheet structures, which believed to be neurotoxic. However, actual secondary structure that contributes most neurotoxicity remains unknown. lack knowledge due challenging nature characterizing amyloids in cells. To overcome this and investigate molecular changes proteins directly cells, we used synchrotron-based...

10.3390/ijms22073430 article EN International Journal of Molecular Sciences 2021-03-26

Alzheimer's disease (AD) is the most common neurodegenerative disease. Most cases of AD are considered idiopathic and likely due to a combination genetic, environmental, lifestyle-related risk factors. Despite occurring decades before typical age an diagnosis, early-life stress (ELS) has been suggested have long-lasting effects that may contribute pathogenesis. Still, mechanisms underlie role ELS on remain largely unknown. Here, we used 5xFAD transgenic mice study relatively short-term...

10.1016/j.bbih.2023.100663 article EN cc-by-nc-nd Brain Behavior & Immunity - Health 2023-07-11

ABSTRACT Alzheimer’s disease (AD) is a progressive neurodegenerative in which the formation of extracellular aggregates amyloid beta (Aβ) peptide, intraneuronal tau neurofibrillary tangles and microglial activation are major pathological hallmarks. One key molecules involved galectin-3 (gal3), we demonstrate here for first time role gal3 AD pathology. Gal3 was highly upregulated brains patients 5xFAD (familial disease) mice, found specifically expressed microglia associated with Aβ plaques....

10.1101/477927 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-12-04
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