Showing papers in "Experimental Neurology in 2003"

TL;DR: Grafted NSCs were genetically modified to produce neurotrophin-3, which significantly expanded NSC effects on host axons and confirmed that grafted stem cells expressed neurotrophic factor genes in vivo.

TL;DR: It is demonstrated that chronic systemic exposure to the pesticide and mitochondrial toxin rotenone through jugular vein cannulation reproduced many features of Parkinson's disease in rats, including nigrostriatal dopaminergic degeneration and formation of alpha-synuclein-positive cytoplasmic inclusions in nigral neurons.

TL;DR: It is suggested that failure of the ubiquitin-proteasome system to adequately clear unwanted proteins may underlie vulnerability and degeneration of the SNc in both sporadic and familial PD.

TL;DR: Combined glial fibrillary acidic protein (GFAP) immunohistochemistry and in situ hybridization demonstrated that GFAP astrocytes constituted a source of neurocan production after spinal cord injury, establishing a CSPG-rich matrix that persists for up to 2 months following injury.

TL;DR: The data indicate that transplanted hATSCs survive, migrate, and improve functional recovery after stroke and that genetically engineered h ATSCs can express biologically active gene products and, therefore, can function as effective vehicles for therapeutic gene transfer to the brain.

TL;DR: Major neuropathological changes not previously studied in the rodent pilocarpine model include widespread microglial activation, delayed thalamic axonal death, and persistent NPY upregulation in mossy fibers, together revealing extensive and persistent glial as well as neuronal pathology.

TL;DR: The results of this study demonstrate that the incorporation of a novel delivery system providing controlled release of growth factors enhances peripheral nerve regeneration and represents a significant contribution toward enhancing nerve regeneration across short nerve gaps.

TL;DR: GFP bone marrow chimeric mice are a powerful tool to further differentiate the function of resident microglia and hematogenous macrophages following cerebral ischemia.

TL;DR: It is demonstrated that oxidative and mitochondrial stress factors are present at several phases of Abeta pathology progression, confirming the neuronal dysfunction in APP transgenic mice.

TL;DR: This study provided the first direct and quantitative evidence that long-term continuous treatment with exogenous GDNF significantly increased the number of motoneurons which regenerate their axons, completely reversing the negative effects of chronic axotomy.

TL;DR: It is proposed that the sequence of OL lineage progression is a useful means to estimate developmental windows of white matter maturation in perinatal rodents that coincide with those of developing human cerebral white matter.

TL;DR: The spatiotemporal pathologies of neuronal, axonal, vascular, and macro- and microglial elements at 1, 4, 7, and 28 days after moderate controlled cortical impact injury are determined and recent evidence that suggests there may be some degree of endogenous repair after central nervous system injury is discussed.

TL;DR: Testing the ability of Ginkgo biloba, a flavonoid-rich antioxidant, to antagonize the age-related behavioral impairment and neuropathology exhibited by Tg2576 mice indicates that chronic Gink go biloba treatment can block an age-dependent decline in spatial cognition.

TL;DR: The results suggest that the neurotrophic properties of OEC may involve secretion of neurotrophic molecules but that cellular interactions are crucial.

TL;DR: Grafts of BDNF + NT-3 expressing fibroblasts delayed 6 weeks after injury elicit growth from intact segmental and descending spinal tracts, stimulate modest regenerative growth by rubrospinal axons, and partially rescue axotomized supraspinal neurons and protect them from atrophy.

TL;DR: It is demonstrated that social environments can modify neurogenesis and synaptic plasticity in adult hippocampal regions, which is associated with alterations in spatial learning and memory.

TL;DR: The results indicate that forced exercise can reduce the vulnerability of dopamine neurons to 6-hydroxydopamine, and raise the possibility that exercise will protect against a variety of neurodegenerative conditions.

TL;DR: In this article, the authors show that transplanted Schwann cells and olfactory ensheathing cells (OECs) create an environment favorable to axon regeneration when transplanted into the damaged spinal cord.

TL;DR: The results suggest that KW-6002 can attenuate the induction as well as the expression of motor response alterations to chronic dopaminergic stimulation in parkinsonian animals, possibly by blocking A(2A) receptor-stimulated signaling pathways.

TL;DR: It is concluded that traumatic brain injury stimulates an increase in proliferation of endogenous neural stem/progenitor cells and that a significant number of these express a neuronal marker.

TL;DR: It is demonstrated that p38 MAPK is activated at early stages of neurofibrillary degeneration in AD hippocampus and the p38 activation may also be linked to neurodegeneration through mechanisms other than neuro fibrillar tangle formation.

TL;DR: Only the simultaneous administration of HNE and H(2)O(2), at concentrations similar to those generated within the first 3 h of Abeta exposure, can fully mimic Abeta-dependent activation of JNKs and p38(MAPK) and occurrence of apoptosis.

TL;DR: During the 54(th) Annual Meeting of the American Academy of Neurology, a group of investigators active in the fields of biomakers, neuroimaging, and neuroprotection met to review the three techniques mentioned above and developed consensus on a set of 10 criteria for a neuroim imaging technique to be considered adequate as a biomarker for progression of PD.

TL;DR: Findings suggest that the augmentation of TGFbeta-1 gene expression and the attenuation of pro-inflammatory cytokine gene expression combined with an altered distribution of activated microglia/macrophages in the re-injured spinal cord might create a more favorable milieu for transplants and axonal regrowth as compared to the acutely injured spinal cord.

TL;DR: It is suggested that intracellular zinc release from MT-III may contribute substantially to zinc-mediated neuronal death in certain brain areas, including the hippocampal CA1 region and the thalamus.

TL;DR: It is concluded that CXCL10 plays a critical role in recruitment of T lymphocytes to sites of spinal cord injury, and that a reduction of T-lymphocyte recruitment significantly enhances tissue preservation and functional outcome.

TL;DR: Growth factor gene delivery can elicit growth of corticospinal axons in chronic stages of injury and improves functional outcomes compared to non-growth-factor-treated animals.

TL;DR: The characteristics of the chronically injured spinal Cord are considered that make it an even more challenging setting in which to elicit regeneration than the acutely injured spinal cord and the treatments that have been designed to enhance axon growth are reviewed.

TL;DR: Analysis of the postnatal development of pathological manifestations of inflammation in several brain regions of NPC1-/- mice suggests that microglial activation precedes and might be causally related to neuronal degeneration, while astrocyte activation might be a consequence of neurons degeneration.

TL;DR: The increased area and density of GAP-43-IR is consistent with neurite sprouting, and the colocalization with alpha-CGRP indicates that some of the sprouting neurites are nociceptive primary afferents.