A5084830099- Alzheimer's disease research and treatments
- Genetic Neurodegenerative Diseases
- Mitochondrial Function and Pathology
- Neuroscience and Neuropharmacology Research
- Neurological Disease Mechanisms and Treatments
- Barrier Structure and Function Studies
- Neurogenesis and neuroplasticity mechanisms
- Cancer-related Molecular Pathways
- Cerebrovascular and genetic disorders
- Medicinal Plants and Neuroprotection
- Trace Elements in Health
- Intracerebral and Subarachnoid Hemorrhage Research
- Drug Transport and Resistance Mechanisms
- Supramolecular Self-Assembly in Materials
- Neurological diseases and metabolism
- Neurological disorders and treatments
- DNA Repair Mechanisms
- Glycosylation and Glycoproteins Research
- Cholinesterase and Neurodegenerative Diseases
- Cell death mechanisms and regulation
- Botulinum Toxin and Related Neurological Disorders
- Dementia and Cognitive Impairment Research
Universitat de Barcelona
2008-2013
Biomedical Research Networking Center on Neurodegenerative Diseases
2008-2013
Late-onset Alzheimer's disease (AD) is the most common form of AD appearing after 65 years age. To date, however, there are no non-genetically manipulated rodent models that develop a similar sporadic onset with age-related amyloid-beta (Abeta) deposition. Although senescence accelerated mouse prone 8 (SAMP8) mice have been proposed as model AD, presence Abeta deposits remains controversial. In this study, we describe time course deposition in SAMP8 well control SAMR1 and ICR-CD1 strains...
Abstract This study was undertaken to investigate the potential role of cell cycle re‐entry in an experimental model Huntington's disease and human brain samples. We found that after treatment rats with mitochondrial neurotoxin 3‐nitropropionic acid, expression markers G1 phase measured by immunohistochemistry induced striatal region. Furthermore, we detected increase nuclear also cytoplasmatic E2F‐1 expression, suggesting this protein could activate apoptotic cascade rat brain. Western blot...
The senescence accelerated mouse-prone 8 (SAMP8) strain of mice is an experimental model that has also been proposed as a Alzheimer's disease it shares several features with this dementia. We have recently report
J. Duran‐Vilaregut, del Valle, G. Manich, A. Camins, M. Pallàs, Vilaplana and C. Pelegrí (2011) Neuropathology Applied Neurobiology 37, 525–537 Role of matrix metalloproteinase (MMP)‐9 in striatal blood–brain barrier disruption a 3‐nitropropionic acid model Huntington's disease Aims: 3‐Nitropropionic (3‐NPA) is natural toxin that, when administered to experimental animals, reproduces the brain lesions observed disease, which mainly consist selective neurodegeneration striatum. The also...
Cerebrovascular dysfunction and β-amyloid peptide deposition on the walls of cerebral blood vessels might be an early event in development Alzheimer’s disease. Here we studied time course amyloid blood-brain barrier (BBB) disruption CA1 subzone hippocampus SAMP8 mice association between these two variables. We also recently described clusters parenchyma, as well with which BBB is disrupted. showed greater than age-matched ICR-CD1 control mice. Moreover, at 12 months age number a disrupted...
Abstract Senescence of the cerebrovascular system and an abnormal function blood–brain barrier have been related with Alzheimer's disease. We studied here time‐course disruption in senescence‐accelerated mouse prone 8 (SAMP8) mice, which is a murine model senescence also considered used previously described method that allows evaluating integrity by observing Evans blue extravasation from brain blood vessels. Three regions (cortex, hippocampus hippocampal fissure) SAMP8 brains were analyzed...
Abstract 3‐Nitropropionic acid (3‐NPA) is a mitochondrial toxin used in the laboratory to replicate neurodegenerative conditions that are accompanied by degeneration of caudate‐putamen. 3‐NPA induces depletion ATP production, reactive oxygen species and secondary excitotoxicity mediated activation N‐methyl‐D‐aspartate receptors culminates triggering cell death mechanisms, including apoptosis. We here examined immunohistochemical methods whether cellular expression phospho Ser1981 ‐ataxia...