A5013205418- Parkinson's Disease Mechanisms and Treatments
- Nerve injury and regeneration
- Neurological disorders and treatments
- Neurogenesis and neuroplasticity mechanisms
- Olfactory and Sensory Function Studies
- Nuclear Receptors and Signaling
- Neurological Disease Mechanisms and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Autism Spectrum Disorder Research
- Prion Diseases and Protein Misfolding
- Medicinal Plants and Neuroprotection
- Neuroscience and Neuropharmacology Research
- Botulinum Toxin and Related Neurological Disorders
- Dementia and Cognitive Impairment Research
- Ubiquitin and proteasome pathways
- Neuroscience of respiration and sleep
- Mesenchymal stem cell research
- Biotin and Related Studies
- NF-κB Signaling Pathways
- Congenital heart defects research
- Tissue Engineering and Regenerative Medicine
- Genetic Neurodegenerative Diseases
- Signaling Pathways in Disease
- Neurological Disorders and Treatments
Universidad de Navarra
2009-2025
Navarre Institute of Health Research
2019-2025
Clinica Universidad de Navarra
2011-2014
Objective Alzheimer disease (AD) is the leading cause of dementia, and although its etiology remains unclear, it seems that type 2 diabetes mellitus (T2DM) other prediabetic states insulin resistance could contribute to appearance sporadic AD. As such, we have assessed whether tau β‐amyloid (Aβ) deposits might be present in pancreatic tissue subjects with AD, amylin, an amyloidogenic protein deposited pancreas T2DM patients, accumulate brain AD patients. Methods We studied from 48...
Increasing evidence suggests a pivotal role for neuroinflammation in the pathogenesis of Parkinson disease, but whether activated microglia participate disease progression remains unclear. To clarify this issue, we determined numbers microglial cells substantia nigra pars compacta and ventral tegmental area monkeys subacutely chronically exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Monkeys subacute MPTP treatment group were killed 1 week after last injection; treated...
Abstract Protein misfolding diseases refer to a variety of disorders that develop as consequence the proteins in various organs. The etiologies Parkinson’s and Alzheimer’s disease remain unclear, but it seems type two diabetes other prediabetic states could contribute appearance sporadic forms these diseases. In addition amylin deposition, amyloidogenic implicated pathophysiology neurodegenerative have important roles pathogenesis this disease. As we previously demonstrated presence...
Abstract We investigated the impact of nigrostriatal lesion on olfactory tyrosine hydroxylase‐immunoreactive (TH‐ir) cells in monkeys. The majority these TH‐ir appeared glomerular layer bulb and many were immature but functional dopaminergic neurons. In parkinsonian monkeys number neurons increased up to 100% as compared controls, their phenotype did not change. This cell population might be a direct consequence nigral loss contribute hyposmia reported by Parkinson's disease patients.Synapse...
In addition to the medium spiny neurons mammalian striatum contains a small population of GABAergic interneurons that are immunoreactive for tyrosine hydroxylase (TH), which dramatically increases after lesions nigrostriatal pathway and striatal delivery neurotrophic factors. The regulatory effect levodopa (L-Dopa) on number phenotype these cells is less well understood. Eleven macaques (Macaca fascicularis) were included. Group I (n = 4) received 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine...
Synucleinopathies are a group of neurodegenerative diseases without effective treatment characterized by the abnormal aggregation alpha-synuclein (aSyn) protein. Changes in levels or amino acid sequence aSyn (by duplication/triplication gene point mutations encoding region) cause familial cases synucleinopathies. However, specific molecular mechanisms aSyn-dependent toxicity remain unclear. Increased protein pathological may favor protein-protein interactions (PPIs) that could either promote...
Abstract We assessed the presence of degenerating neurons in substantia nigra pars compacta (SNpc) and ventral tegmental area (VTA) parkinsonian monkeys. For this purpose, we used two histological markers cellular death, Fluoro Jade B (FJB) staining terminal deoxynucleotidyl transferase‐mediated dUTP nick end labelling (TUNEL). Eight monkeys were subacutelly treated with four to six 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) injections (1–1.5 mg/kg, cumulative dose) sacrificed 1...
To elucidate the role of prostaglandin synthase cyclooxygenase-2 (Cox-2) and mechanisms dopaminergic (DA) neurodegeneration, monkeys were injected subacutely or chronically (n = 5/group) with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Chronically treated animals developed parkinsonian signs killed 6 months after last treatment; tyrosine hydroxylase-expressing neurons decreased in all substantia nigra (SN) cell groups both treatment groups. In untreated controls 3), there was low Cox-2...