Showing papers in "Neurobiology of Disease in 2004"

TL;DR: The pathogenesis of increased BBB permeability in hypoxia-ischemia and inflammatory mechanisms involving the BBB in septic encephalopathy, HIV-induced dementia, multiple sclerosis, and Alzheimer disease are described.

TL;DR: The findings indicate that cerebral microglial activation can be detected in vivo during the evolution of ALS, and support the previous observations that cerebral pathology is widespread, and argue for the development of therapeutic strategies aimed at inflammatory pathways.

TL;DR: By indulging into the molecular mechanisms that cause oligodendrocyte apoptosis and identifying potential targets for therapeutic intervention, the prevention of this apoptotic wave will be of tremendous value to individuals living with SCI.

TL;DR: Animal models of glutamate transporter dysfunction have revealed a significant role for these proteins in pathologic conditions such as neurodegenerative diseases, epilepsy, stroke, and central nervous system tumors.

TL;DR: The mouse model of L-DOPA-induced dyskinesia will provide a useful tool to study the molecular determinants of this movement disorder in transgenic mice strains and it is concluded that 6-OHDA lesioned mice exhibit behavioral and cellular features of akinesia and L- DOPA- induced dysKinesia that are similar to those previously characterized in rats.

TL;DR: It is hypothesized that neuroapoptotic damage in homologous regions of human brain underlies cognitive deficits in FAS and the human brain of FAS victims has a similar capacity to effect functional recovery.

TL;DR: In this article, the effects of chronic epilepsy on dentate neurogenesis were investigated by quantifying the number of cells that are positive for doublecortin (DCX, a marker of new neurons) in adult F344 rats at 16 days and 5 months after an intracerebroventricular kainic acid (ICV KA) administration or after graded intraperitoneal KA (IP KA), models of temporal lobe epilepsy (TLE).

TL;DR: It is shown that the brain levels of both 3-HK and QUIN are increased three to four-fold in low-grade HD brain, and changes were seen in the neocortex and in the neostriatum, but not in the cerebellum.

TL;DR: Results add to the evidence that kynurenine pathway changes might be involved in the pathogenesis of schizophrenia and the schizophrenia-like psychoses of other disorders.

TL;DR: It is reported that short exposures to nonphysiologic oxygen levels can trigger apoptotic neurodegeneration in the brains of infant rodents, and the synRas-transgenic mice overexpressing constitutively activated Ras and phosphorylated kinases ERK1/2 in the brain were protected against oxygen neurotoxicity.

TL;DR: Although pro-inflammatory markers were induced in a different manner across the CNS, their patterns were not characteristic of those caused by other inflammatory challenges, such as endotoxin, which suggest a different mechanism involved in regulating the innate immune reaction in response to seizures.

TL;DR: The data support the use of minocycline in parkinsonian patients if inflammation is proved to be involved in the ethiopathology of Parkinson's disease, and potential involvement of lipopolysaccharide-induced formation of peroxynitrites and cytokines in the pathological events in substantia nigra in response to inflammation is discussed.

TL;DR: The different alpha-synuclein transgenic models are described, their clinical relevance to synucleinopathies, and their further utilization to understand the disease process are described.

TL;DR: It is demonstrated that inhibition of anti-Aβ antibody-induced microglial activation with anti-inflammatory drugs, such as dexamethasone, inhibits removal of fibrillar amyloid deposits, and this activation may result in an impaired clinical response to vaccination against Aβ.

TL;DR: This characterization of PPT1-/- mice not only provides defined pathological landmarks for understanding disease pathogenesis, but also provides an invaluable resource for subsequently judging the efficacy of therapeutic strategies.

TL;DR: It is suggested that augmenting SVZ neuroblast recruitment and survival may improve neural repair after neonatal brain injury, and increase in the SVZ area correlated directly with the degree of hemispheric damage.

TL;DR: The results suggest that as amyloid beta (Abeta) deposition and levels increase over time in PDAPP mice, these changes lead to primary or secondary white matter injury that can be detected by DTI.

TL;DR: Investigation of the effectiveness of transplantation of human neural stem cells into adult rat striatum prior to induction of striatal damage with the mitochondrial toxin 3-nitropropionic acid shows that proactive transplanted hNSCs protect host striatal neurons against neuronal injury and improve motor impairment induced by 3-NP toxicity.

TL;DR: The results show that this model is capable of reproducing major biochemical and neurological changes of diffuse clinical TBI, and has been described as a newly developed, highly controlled, and reproducible model.

TL;DR: Results indicate that proteins and their proteolytic fragments released from degenerating neurons are cerebrospinal fluid markers for acute brain damage and suggest that efflux of proteins from the injured brain may reflect underlying mechanisms for neurodegeneration.

TL;DR: It is suggested that gamma-secretase is a heterogeneous family of protein complexes widely expressed in the adult organism and several independent gamma- secretase complexes can coexist in the same cell type.

TL;DR: It is shown that systemic administration of the NMDA receptor antagonist MK801 to 7-day-old rats leads to impaired activity of extracellular signal-regulated kinase 1/2 (ERK1/2) and reduces levels of phosphorylated cAMP-responsive element binding protein (CREB) in brain regions which display severe apoptotic neurodegeneration.

TL;DR: In rats that developed dyskinesia, GABA neurons had an increased transcriptional activity, and genes involved in Ca2+ homeostasis, inCa2+ -dependent signaling, and in structural and synaptic plasticity were upregulated.

TL;DR: The demonstration that treatment with miglustat, which has no direct effect on cholesterol metabolism, corrects the abnormal lipid trafficking seen in B lymphocytes in NP-C indicates that glycosphingolipid accumulation is the primary pathogenetic event inNP-C.

TL;DR: The present review summarizes the available data supporting the clinical testing of minocycline for Huntington's disease, amyotrophic lateral sclerosis and Parkinson's disease and extends the discussion to the potential applications of minicelline for combining this treatment with cellular and molecular therapy.

TL;DR: The results suggest that the dose and timing of IGF-I administration are critical for producing a neuroprotective effect, and also suggest that both the MAPK and PI-3K/Akt pathways can promote the survival of motor neurons.

TL;DR: A medium-throughput cell-based assay to screen drugs for Huntington's disease (HD), which measures the ability of drugs to protect cultured neuronal cells from death caused by an expanded polyglutamine form of huntingtin exon 1.

TL;DR: The data suggest that seizure-related IL1-beta, NF-kappaB, and COX-2 expression may contribute to the pathophysiology of epilepsy by inducing neuronal death and astrocytic activation.

TL;DR: TPPP/p25 seems to be a novel marker of alpha-synucleinopathies, associated with microtubules in vitro and can induce the formation of aberrant microtubule assemblies in Alzheimer's disease (AD).

TL;DR: The findings suggest that NDRG2 upregulation is associated with disease pathogenesis in the human brain and provide new insight into the molecular changes that occur in AD.