Javier Blesa

ORCID: 0000-0002-4257-1325
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About
Contact & Profiles
Research Areas
  • Parkinson's Disease Mechanisms and Treatments
  • Neurological disorders and treatments
  • Nerve injury and regeneration
  • Neuroscience and Neuropharmacology Research
  • Neurological diseases and metabolism
  • Botulinum Toxin and Related Neurological Disorders
  • Autism Spectrum Disorder Research
  • Ultrasound and Hyperthermia Applications
  • Nuclear Receptors and Signaling
  • Genetic Neurodegenerative Diseases
  • Neurotransmitter Receptor Influence on Behavior
  • Alzheimer's disease research and treatments
  • Bacteriophages and microbial interactions
  • SARS-CoV-2 and COVID-19 Research
  • Advanced MRI Techniques and Applications
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Monoclonal and Polyclonal Antibodies Research
  • Lysosomal Storage Disorders Research
  • Protein Degradation and Inhibitors
  • Diet and metabolism studies
  • Peptidase Inhibition and Analysis
  • Photoacoustic and Ultrasonic Imaging
  • Neuroscience and Neural Engineering
  • RNA regulation and disease
  • Neurogenesis and neuroplasticity mechanisms

Biomedical Research Networking Center on Neurodegenerative Diseases
2015-2025

HM Hospitales
2015-2025

University Hospital HM Puerta del Sur
2016-2025

Centro de Investigación Biomédica en Red
2009-2025

Instituto de Salud Carlos III
2018-2025

Camilo José Cela University
2024-2025

Universidad Internacional
2024

Ibero American University
2024

Ibero-American University Puebla
2024

Research Network (United States)
2023-2024

Mounting evidence suggests that α-synuclein, a major protein component of Lewy bodies (LB), may be responsible for initiating and spreading the pathological process in Parkinson disease (PD). Supporting this concept, intracerebral inoculation synthetic recombinant α-synuclein fibrils can trigger pathology mice. However, it remains uncertain whether pathogenic effects apply to PD-linked occur species closer humans.Nigral LB-enriched fractions containing were purified from postmortem PD brains...

10.1002/ana.24066 article EN Annals of Neurology 2013-11-16

The development of new therapies to slow down or halt the progression Parkinson's disease is a health care priority. A key pathological feature presence alpha-synuclein aggregates, and there increasing evidence that propagation plays central role in progression. Consequently, downregulation potential therapeutic target. As chronic disease, ideal treatment will be minimally invasive effective long-term. Knockdown gene expression has clear potential, siRNAs specific have been designed;...

10.1016/j.ymthe.2019.08.010 article EN cc-by-nc-nd Molecular Therapy 2019-08-27

Abstract Age-related neurodegenerative diseases involving amyloid aggregation remain one of the biggest challenges modern medicine. Alterations in gastrointestinal microbiome play an active role aetiology neurological disorders. Here, we dissect amyloidogenic properties biofilm-associated proteins (BAPs) gut microbiota and their implications for synucleinopathies. We demonstrate that BAPs are naturally assembled as amyloid-like fibrils insoluble fractions isolated from human microbiota. show...

10.1038/s41467-024-48309-x article EN cc-by Nature Communications 2024-05-16

The cause of degeneration nigrostriatal dopamine (DA) neurons in idiopathic Parkinson's disease (PD) is still unknown. Intraneuronally, DA largely confined to synaptic vesicles where it protected from metabolic breakdown. In the cytoplasm, however, free can give rise formation cytotoxic radicals. Normally, concentration cytoplasmic kept at a minimum by continuous pumping activity vesicular monoamine transporter (VMAT)2. Defects handling cytosolic VMAT2 increase levels DA-generated oxy...

10.1523/jneurosci.5456-13.2014 article EN Journal of Neuroscience 2014-06-11

Abstract Background Parkinson's disease (PD) exhibits a high prevalence of dementia as severity and duration progress. Focused ultrasound (FUS) has been applied for transient blood–brain barrier (BBB) opening cortical regions in neurodegenerative disorders. The striatum is primary target delivery putative therapeutic agents PD. Objective Here, we report prospective, single‐arm, nonrandomized, proof‐of‐concept, phase I clinical trial (NCT03608553 amended) PD with to test the safety...

10.1002/mds.29134 article EN Movement Disorders 2022-06-28

Intracerebral vector delivery in nonhuman primates has been a major challenge. We report successful blood-brain barrier opening and focal of adeno-associated virus serotype 9 vectors into brain regions involved Parkinson’s disease using low-intensity focus ultrasound adult macaque monkeys. Openings were well tolerated with generally no associated abnormal magnetic resonance imaging signals. Neuronal green fluorescent protein expression was observed specifically confirmed opening. Similar...

10.1126/sciadv.adf4888 article EN cc-by-nc Science Advances 2023-04-19

Accumulating evidence from genetic and biochemical studies implicates dysfunction of the autophagic-lysosomal pathway as a key feature in pathogenesis Parkinson's disease (PD). Most have focused on accumulation neurotoxic α-synuclein secondary to defects autophagy cause neurodegeneration, but abnormalities system likely mediate toxicity through multiple mechanisms. To further explore how endolysosomal causes PD-related we generated murine model Kufor-Rakeb syndrome (KRS), characterized by...

10.1523/jneurosci.0632-14.2015 article EN cc-by-nc-sa Journal of Neuroscience 2015-04-08

Despite unprecedented global efforts to rapidly develop SARS-CoV-2 treatments, in order reduce the burden placed on health systems, situation remains critical. Effective diagnosis, treatment, and prophylactic measures are urgently required meet demand: recombinant antibodies fulfill these requirements have marked clinical potential. Here, we describe fast-tracked development of an alpaca Nanobody specific for receptor-binding-domain (RBD) Spike protein with potential therapeutic...

10.1038/s41598-021-82833-w article EN cc-by Scientific Reports 2021-02-08

Abstract The recent knowledge that 10 years after transplantation surviving human fetal neurons adopt the histopathology of Parkinson's disease suggests Lewy body formation takes a decade to achieve. To determine whether similar occurs in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐primate models over timeframe, brains two adult monkeys made parkinsonian their youth with intermittent injections MPTP were studied. Despite substantial nigral degeneration and increased α‐synuclein...

10.1002/mds.22481 article EN Movement Disorders 2009-06-12
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