Showing papers in "Neurobiology of Disease in 2005"

TL;DR: C cognition in 6- and 18-month old transgenic mice expressing APPswe and PS1dE9 is examined, finding that some form of Abeta associated with amyloid deposition can disrupt cognitive circuits when the cholinergic and somatostatinergic systems remain relatively intact; and that episodic-like memory seems to be more sensitive to the toxic effects of Abetas.

TL;DR: It is reported that cultured Tg2576 APP mutant neurons have selective alterations in pre- and post-synaptic compartments compared to wild-type neurons, and evidence is provided that Abeta is specifically involved in these alterations in synaptic biology.

TL;DR: The results support the view of a potential neuroprotective action of cannabinoids against the in vivo and in vitro toxicity of 6-hydroxydopamine, which might be relevant to Parkinson's disease (PD).

TL;DR: It is shown that trehalose is also effective in inhibiting aggregation of Abeta and reducing its cytotoxicity, although it shows differential effects toward Abeta40 and Abeta42.

TL;DR: The data suggest that the macrophage response to toxin-induced demyelination influences the growth factor environment, thereby affecting the behavior of OPCs and hence the efficiency of remyelinations.

TL;DR: It is suggested that infiltration of BM-derived monocytic cells into the brain contributes to the development of microglial reaction in AD.

TL;DR: The results suggest that oligomers induced a profound, early inflammatory response, whereas fibrillar Abeta showed less increase of pro-inflammatory molecules, consistent with a more chronic form of inflammation.

TL;DR: Results show that NGF does not alter platination of DNA, indicating that it interrupts the platinum death pathway after adduct formation, and disproportionate platinum accumulation may explain why a drug aimed at killing rapidly dividing cells causes sensory neurotoxicity.

TL;DR: It is supported that ES cell transplantation and gene modification may have values for enhancing recovery after stroke and further increased the survival of transplanted ES cells, neuronal differentiation, and functional outcome.

TL;DR: These results provide the first large scale description of gene expression profiles of dopamine neurons and suggest several avenues for investigation into dopaminergic neuroprotective therapy for PD.

TL;DR: Mice with a selective deletion of PrP(C) exhibited deficits in hippocampal-dependent spatial learning, but non-spatial learning remained intact, and deficits were seen in mPrP-/- mice with a homogeneous 129/Ola background and in m prisoners in the mixed mix indicating that these abnormalities were unlikely due to variability of background genes or alteration of the nearby Prnd (doppel) gene.

TL;DR: A progressive decrease in the number of proliferating cells in the dentate gyrus of R6/2 mice was found and corresponded to a reduction in actual hippocampal neurogenesis as assessed by double immunostaining for BrdU and the neuronal marker neuronal nuclei (NeuN).

TL;DR: It is shown for the first time that in MS brain changes in the vasculature take place not only in focal lesions but also in DAWM as detected by postmortem MRI.

TL;DR: Transplantation of neural precursors by a variety of routes can deliver cells with the potential to replace injured neurons to ischemic brain regions and enhance their migration when delivered by any of these routes.

TL;DR: Proteomic analysis of transgenic mice overexpressing A30P alpha-synuclein suggests proteins associated with impaired energy metabolism and mitochondria are particularly prone to oxidative stress associated with A 30P-mutant alpha- Synuclein.

TL;DR: These findings challenge the idea that tau pathology in Alzheimer's disease is merely a downstream effect of amyloid production/deposition and suggest that reciprocal interactions between beta-amyloid and tau alterations may take place in vivo.

TL;DR: This study suggests that water-soluble Coenzyme Q10 acts by stabilizing the mitochondrial membrane when neuronal cells are subjected to oxidative stress, and has the potential to be used as a therapeutic intervention for neurodegenerative diseases.

TL;DR: Modifications in the expression of constitutive Dyrk1A in the cytoplasm and nuclei of neurons in various neurodegenerative diseases associated with tau phosphorylation are indicated.

TL;DR: Exposure to PQ with or without MB induces neurodegeneration which might occur via an early inflammatory response in young adult animals, indicating that Parkinson's disease prevalence in rural environments where pesticides are widely used is increasing.

TL;DR: Findings demonstrate distinct roles for PDGF and FGF2 in vivo in the context of a demyelinating disease with spontaneous remyelination and impaired oligodendrocyte regeneration of PDGF alpha R heterozygotes.

TL;DR: It is demonstrated that impaired Cu/Zn-SOD activity contributes to oxidative damage in Thy1-APP751(SL) transgenic mice, and these findings are closely linked to increased beta-amyloidogenic cleavage of APP.

TL;DR: Findings suggest that the increased brain inflammation in apoE4 mice is related to disregulation of NF-kappaB signaling pathway.

TL;DR: Evidence is provided that PrPc deficiency increases infarct size by approximately 200%, while transgenic PrPC restores tissue viability, albeit not above levels in wild-type animals, and data suggest a role of cytosolic signaling pathways in Prnp(0/0)-induced cell death.

TL;DR: Findings suggest that defective calcium homeostasis may be a mechanism responsible for neuropathophysiology in acute neuronopathic Gaucher disease, and may potentially offer new therapeutic approaches for disease management.

TL;DR: It is demonstrated that neural progenitors proliferate in chronic epilepsy and suggested that the fissura hippocampi behaves like another neurogenic area.

TL;DR: The results suggest that MS lymphocytes show a complex pattern of gene regulation that represents a counterbalance between promoting and preventing apoptosis and DNA damage of lymphocytes.

TL;DR: It is found that developmental seizures promote co-assembly of hippocampal HCN1/HCN2 heteromeric channels, in a duration-dependent manner, which suggests that heteromersic HCN channels may provide molecular targets for intervention in the epileptogenic process.

TL;DR: Reduction of endocannabinoid signaling is associated with the development of EAE in rats and the direct or indirect activation of vanilloid or cannabinoid receptors may reduce the neurological impairment experienced by EAE rats, although the efficacy of the different compounds examined seems to be determined by their particular pharmacodynamic and pharmacokinetic characteristics.

TL;DR: To the knowledge, this is the first study to suggest that cognitive deficits in APOE*4 carriers are due to inherent defects in synaptic function that appear prior to any age-dependent markers of neuropathology.

TL;DR: The present findings show novel mechanisms for the neuroprotective effects of citicoline, which cooperate to decrease brain glutamate release after ischemia.