Enhancement of immunoreactivity for NF-κB in the hippocampal formation and cerebral cortex of Alzheimer's disease

Terai, Kazuhiro; Matsuo, Akinori; McGeer, Patrick L.

doi:10.1016/0006-8993(96)00310-1

Cited by 193 publications

(63 citation statements)

References 37 publications

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“…Functional NF-B dimers are present in essentially all cell types in the CNS, including neurons, astro- cytes, microglia, and oligodendrocytes (O'Neill and . In AD brains, NF-B immunoreactivity is greater in neurons and astrocytes surrounding amyloid plaques (Terai et al, 1996;Kaltschmidt et al, 1997). Additionally, it has been reported that A␤ stimulation leads to NF-B activation in cultured neurons and glia (Akama et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Medeiros¹,

Prediger²,

Passos³

et al. 2007

J. Neurosci.

270

179

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Section: Discussionmentioning

confidence: 99%

Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Medeiros¹,

Prediger²,

Passos³

et al. 2007

J. Neurosci.

270

179

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“…Expression of NF-B (p65) in brain has already been reported in neurons of the SN and other brain regions, including the hippocampus, striatum, and cerebral cortex of the rat (27), and in the hippocampus and the entorhinal cortex of control subjects and patients with Alzheimer disease (28). In these studies, as in ours, NF-B was localized, for the most part, in the cytoplasm, indicating that it is not constitutively activated, even in pathological human brain.…”

Section: Discussionmentioning

confidence: 84%

Nuclear translocation of NF-κB is increased in dopaminergic neurons of patients with Parkinson disease

Hunot

Brugg

Ricard

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

653

402

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Evidence from postmortem studies suggest an involvement of oxidative stress in the degeneration of dopaminergic neurons in Parkinson disease (PD) that have recently been shown to die by apoptosis, but the relationship between oxidative stress and apoptosis has not yet been elucidated. Activation of the transcription factor NF-B is associated with oxidative stress-induced apoptosis in several nonneuronal in vitro models. To investigate whether it may play a role in PD, we looked for the translocation of NF-B from the cytoplasm to the nucleus, evidence of its activation, in melanized neurons in the mesencephalon of postmortem human brain from five patients with idiopathic PD and seven matched control subjects. In PD patients, the proportion of dopaminergic neurons with immunoreactive NF-B in their nuclei was more than 70-fold that in control subjects. A possible relationship between the nuclear localization of NF-B in mesencephalic neurons of PD patients and oxidative stress in such neurons has been shown in vitro with primary cultures of rat mesencephalon, where translocation of NF-B is preceded by a transient production of free radicals during apoptosis induced by activation of the sphingomyelindependent signaling pathway with C 2

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“…Previous studies have reported that inappropriate regulation of NF-kB/Rel-mediated transcription is associated with pathological conditions including acute inflammatory responses, toxic/septic shock, acute phase reactions, atherosclerosis, radiation damage, and also with several neuropathologies (Grilli et al, 1993;Baldwin, 1996;O'Neill and Kaltschmidt, 1997). In post-mortem tissue from patients with neurodegenerative disease or cultured Expression profiling of NMDA receptor antagonists in brain M Marvanová et al neurons exposed to neurotoxic stimuli, increased NF-kB activity in cells has been reported (Kaltschmidt et al, 1995;Terai et al, 1996;Hunot et al, 1997). Furthermore, several studies have demonstrated that stimulation of both NMDA and non-NMDA glutamate receptors strongly stimulate NF-kB in vitro (Guerrini et al, 1995;Kaltschmidt et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Identification of Genes Regulated by Memantine and MK-801 in Adult Rat Brain by cDNA Microarray Analysis

Marvanová

Lakso

Wong

2004

Neuropsychopharmacol

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In this study, we monitored gene expression profiles using cDNA microarrays after an acute systemic administration of the high affinity N-methyl-D-aspartate (NMDA) uncompetitive antagonist MK-801 (1 mg/kg; 4 h), and the clinically used moderate affinity antagonist memantine (25 mg/kg; 4 h) in adult rat brains. From a microarray containing 1090 known genes, 13 genes were regulated by both treatments of which 12 were upregulated and one was downregulated. In addition, 28 and 34 genes were regulated (X1.5-or p0.67-fold change) by either memantine or MK-801, respectively. Genes commonly regulated by both treatments and not previously reported were confirmed by in situ hybridization (ISH) and include regenerating liver inhibitory factor-1 (RL/IF-1), GDP-dissociation inhibitor 1 (GDI-1), neural visinin Ca 2 þ -binding protein 2 (NVP-2), neuromedin B receptor, and Na þ /K þ transporting ATPase 2b. ISH with memantine (5-50 mg/kg) revealed regulation of these genes in other cortical and hippocampal regions. RL/IF-1 induction occurred at 1 h and returned to basal levels by 8 h, consistent with the profile of an immediate early gene. Western blot analysis showed increases (B30-65%) in GDI-1 protein present in both cytosolic and membrane fractions that were significant in the 84-kDa Rab bound form, suggesting that memantine influences Ras-like GTPase function. Genes regulated by a 5 mg/kg dose of memantine might be important in its therapeutic effects. These findings increase the number of known, differentially altered genes after treatment of uncompetitive NMDA receptor antagonists and suggest broader actions of these agents than previously realized.

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Enhancement of immunoreactivity for NF-κB in the hippocampal formation and cerebral cortex of Alzheimer's disease

Cited by 193 publications

References 37 publications

Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Nuclear translocation of NF-κB is increased in dopaminergic neurons of patients with Parkinson disease

Identification of Genes Regulated by Memantine and MK-801 in Adult Rat Brain by cDNA Microarray Analysis

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