Marta Bolós

ORCID: 0000-0003-2652-8607
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Nerve injury and regeneration
  • Neuroscience and Neuropharmacology Research
  • Neurological Disease Mechanisms and Treatments
  • Cholinesterase and Neurodegenerative Diseases
  • Growth Hormone and Insulin-like Growth Factors
  • Tryptophan and brain disorders
  • Axon Guidance and Neuronal Signaling
  • Neurological Disorders and Treatments
  • Neuroblastoma Research and Treatments
  • Thyroid Disorders and Treatments
  • Chemokine receptors and signaling
  • Medicinal Plants and Neuroprotection
  • Epigenetics and DNA Methylation
  • Ubiquitin and proteasome pathways
  • Regulation of Appetite and Obesity
  • Immune cells in cancer
  • Barrier Structure and Function Studies
  • Metabolism, Diabetes, and Cancer
  • Advanced Glycation End Products research
  • Adipose Tissue and Metabolism
  • Neonatal Health and Biochemistry
  • S100 Proteins and Annexins

Centro de Biología Molecular Severo Ochoa
2015-2022

Universidad Autónoma de Madrid
2006-2022

Biomedical Research Networking Center on Neurodegenerative Diseases
2011-2020

Consejo Superior de Investigaciones Científicas
2006-2019

Instituto de Salud Carlos III
2015-2017

Centro de Investigación Biomédica en Red
2017

University of Tasmania
2013-2016

Research Institute Hospital 12 de Octubre
2011-2014

Instituto Cajal
2007-2010

The microtubule-associated protein (MAP) tau plays a critical role in the pathogenesis of tauopathies. Excess can be released into extracellular medium physiological or pathological manner to internalized by surrounding neurons-a process that contributes spread this throughout brain. Such spreading may correlate with progression abovementioned diseases. In addition neurons, other cells. Here we demonstrate microglia take up vitro and vivo. regard, from primary cultures soluble (human...

10.3233/jad-150704 article EN Journal of Alzheimer s Disease 2016-01-08

Extracellular Tau is toxic for neighboring cells, and it contributes to the progression of AD. The CX3CL1/CX3CR1 axis an important neuron/microglia communication mechanism.We studied clearance by microglia both in vitro (microglia primary cultures treated with Cy5-Tau, affinity chromatography study binding CX3CR1, Tau-CX3CL1 competition assays) vivo (stereotaxic injection Cy5-Tau into WT CX3CR1-/- mice). expression CX3CL1 microglial phagocytic phenotype were brain tissue samples from AD...

10.1186/s13024-017-0200-1 article EN cc-by Molecular Neurodegeneration 2017-08-15

Tau is a microtubule-associated protein that expressed in neurons. However, group of neurodegenerative diseases named tauopathies - characterized by an increase aggregated and/or hyperphosphorylated the accumulates inside other cells, such as astrocytes and microglia. Given these glial cells do not produce Tau, its presence can be explained internalization from extracellular medium consequent formation aggregates. Among mechanisms, heparan sulfate proteoglycans (HSPGs) have been proposed to...

10.3389/fnins.2019.00442 article EN cc-by Frontiers in Neuroscience 2019-05-01

Microglia are immune cells that play a crucial role in maintaining brain homeostasis. Among the mechanisms of communication between microglia and neurons, CX3CL1/CX3CR1 axis exerts central modulatory role. Animals lacking CX3CR1 microglial receptor (CX3CR1−/− mice) exhibit marked alterations not only but also neurons located various regions brain. Here we show depletion leads to deficient synaptic integration adult-born granule dentate gyrus (DG), both at afferent efferent level. Regarding...

10.1016/j.bbi.2017.10.002 article EN cc-by-nc-nd Brain Behavior and Immunity 2017-10-12

Alzheimer's disease (AD) is a progressive neurodegenerative associated with senile amyloid-β (Aβ) plaques, neuronal death, and cognitive decline. Neurogenesis in the adult hippocampus, which notably affected by neurodegeneratio

10.3233/jad-2011-102070 article EN Journal of Alzheimer s Disease 2011-04-22

Alzheimer's disease (AD) is a neurodegenerative characterized by the presence of neurofibrillary tangles, constituted tau protein, and plaques formed amyloid-beta protein. The courses with high neural damage, which leads to memory loss death. Here we analyzed CX3CL1, chemokine expressed neurons, in cerebrospinal fluid (CSF) samples from control subjects patients mild cognitive impairment AD dementia. CX3CL1 was decreased CSF dementia compared subjects. However, there not difference plasma same

10.3389/fnins.2018.00609 article EN cc-by Frontiers in Neuroscience 2018-09-07

Heme oxygenase-1 (HO-1), the inducible enzyme responsible for rate-limiting step in heme catabolism, is expressed AIDS-Kaposi sarcoma (KS) lesions. Its expression up-regulated by Kaposi sarcoma-associated herpesvirus (KSHV) endothelial cells, but mechanisms underlying KSHV-induced HO-1 are still unknown. In this study we investigated whether oncogenic G protein-coupled receptor (KSHV-GPCR or vGPCR), one of key KSHV genes involved KS development, activated expression. Here show that vGPCR...

10.1074/jbc.m512199200 article EN cc-by Journal of Biological Chemistry 2006-02-14

Abstract Tau is a neuronal microtubule-associated protein with countless physiological functions. Although the detrimental effects of insoluble aggregated have been widely studied, recent evidence supports notion that soluble (composed mostly monomers and dimers) also toxic for neurons. Here we evaluated long-term impact single stereotaxic injection human on hippocampal granule neurons in mice. At ultrastructural level, reduced number afferent synapses caused dramatic depletion synaptic...

10.1038/s41398-017-0013-6 article EN cc-by Translational Psychiatry 2017-12-06

The amyloid precursor protein (APP) is well studied for its role in Alzheimer disease. However, little known about normal function. In this study, we examined the of APP neural stem/progenitor cell (NSPC) proliferation. NSPCs derived from APP-overexpressing Tg2576 transgenic mice proliferated more rapidly than corresponding background strain (C57Bl/6xSJL) wild-type mice. contrast, knock-out (APP-KO) had reduced proliferation rates when compared with (C57Bl/6). A secreted factor, identified...

10.1074/jbc.m112.443671 article EN cc-by Journal of Biological Chemistry 2013-05-14

Reduced brain input of serum insulin-like growth factor I (IGF-I), a potent neurotrophic peptide, may be associated with neurodegenerative processes. Thus, analysis the mechanisms involved in passage blood-borne IGF-I into shed light onto pathological neurodegeneration and provide new drug targets. A site entrance is choroid plexus. The transport mechanism for this specialized epithelium involves receptor membrane multicargo transporter megalin/LRP2. We have now analyzed process greater...

10.1074/jbc.m109.096594 article EN cc-by Journal of Biological Chemistry 2010-03-30

Alzheimer's disease (AD) and other tauopathies are histopathologically characterized by tau aggregation, along with a chronic inflammatory response driven microglia. Over the past few years, role of microglia in AD has been studied mainly relation to amyloid-β (Aβ) pathology. Consequently, there is substantial knowledge gap concerning molecular mechanisms involved tau-mediated toxicity neuroinflammation, thus hindering development therapeutic strategies. We previously demonstrated that...

10.1007/s12035-021-02715-0 article EN cc-by Molecular Neurobiology 2022-01-10

Vascular endothelial growth factor (VEGF) promotes neurogenesis in the adult hippocampus, but way which this process occurs Alzheimer's disease (AD) brain is still unknown. We examined proliferation of neuronal precursors with an ex

10.3233/jad-2011-111646 article EN Journal of Alzheimer s Disease 2012-03-02
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