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1
Combinational chelation therapy abrogates lead-induced neurodegeneration in rats
2009-10-15

Lead, a ubiquitous and potent neurotoxicant causes oxidative stress which leads to numerous neurobehavioral and physiological alterations. The ability of lead to bind sulfhydryl groups or compete with calcium could be one of the reasons for its debilitating effects. In the present study, we addressed: i) if chelation therapy could circumvent the altered oxidative stress and prevent neuronal ...

Energy Citations Database

2
Dissecting the involvement of tropomyosin-related kinase A and p75 neurotrophin receptor signaling in NGF deficit-induced neurodegeneration
2010-06-21

NGF, the principal neurotrophic factor for basal forebrain cholinergic neurons (BFCNs), has been correlated to Alzheimer's disease (AD) because of the selective vulnerability of BFCNs in AD. These correlative links do not substantiate a comprehensive cause�effect mechanism connecting NGF deficit to overall AD neurodegeneration. A demonstration that neutralizing NGF activity ...

PubMed Central

3
Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice.
2011-03-07

Ethanol exposure during developmental synaptogenesis can lead to brain defects referred to as fetal alcohol syndrome (FAS), which can include mental health problems such as cognitive deficits and mental retardation. In FAS, widespread neuronal death and brain mass loss precedes behavioral and cognitive impairments in adulthood. Because tissue plasminogen activator (tPA) has been implicated in ...

PubMed

4
Apoptosis in transgenic mice expressing the P301L mutated form of human tau.

The rTg4510 mouse is a tauopathy model, characterized by massive neurodegeneration in Alzheimer's disease (AD)-relevant cortical and limbic structures, deficits in spatial reference memory, and progression of neurofibrillary tangles (NFT). In this study, we examined the role of apoptosis in neuronal loss and associated tau pathology. The results showed that DNA fragmentation ...

PubMed

5
Apoptosis in Transgenic Mice Expressing the P301L Mutated Form of Human Tau
2008-03-27

The rTg4510 mouse is a tauopathy model, characterized by massive neurodegeneration in Alzheimer�s disease (AD)-relevant cortical and limbic structures, deficits in spatial reference memory, and progression of neurofibrillary tangles (NFT). In this study, we examined the role of apoptosis in neuronal loss and associated tau pathology. The results showed that DNA fragmentation ...

PubMed Central

6
Therapeutic immunization protects dopaminergic neurons in a mouse model of Parkinson's disease.
2004-06-14

Degeneration of the nigrostriatal dopaminergic pathway, the hallmark of Parkinson's disease, can be recapitulated in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice. Herein, we demonstrate that adoptive transfer of copolymer-1 immune cells to MPTP recipient mice leads to T cell accumulation within the substantia nigra pars compacta, suppression of microglial activation, and ...

PubMed

7
Neuronal selenoprotein expression is required for interneuron development and prevents seizures and neurodegeneration
2010-03-01

Cerebral selenium (Se) deficiency is associated with neurological phenotypes including seizures and ataxia. We wanted to define whether neurons require selenoprotein expression and which selenoproteins are most important, and explore the possible pathomechanism. Therefore, we abrogated the expression of all selenoproteins in neurons by genetic inactivation of the ...

PubMed Central

8
Neurodegeneration with Brain Iron Accumulation

NINDS Neurodegeneration with Brain Iron Accumulation Information Page Skip secondary menu Home Disorders A - Z Neurodegeneration with Brain Iron Accumulation Information Page Publications Organizations News ...

MedlinePLUS

9
S-nitrosylation of Drp1 mediates beta-amyloid-related mitochondrial fission and neuronal injury.
2009-04-01

Mitochondria continuously undergo two opposing processes, fission and fusion. The disruption of this dynamic equilibrium may herald cell injury or death and may contribute to developmental and neurodegenerative disorders. Nitric oxide functions as a signaling molecule, but in excess it mediates neuronal injury, in part via mitochondrial fission or fragmentation. However, the underlying mechanism ...

PubMed

10
Protection against A?-mediated rapid disruption of synaptic plasticity and memory by memantine.
2009-05-14

Soluble amyloid-? protein (A?) may cause cognitive impairment in Alzheimer's disease in the absence of significant neurodegeneration. Here, the ability of the NMDA receptor (NMDAR) antagonist memantine to prevent synthetic A?-mediated rapid functional deficits in learned behavior and synaptic plasticity was assessed in the rat. In vitro, pretreatment with a clinically ...

PubMed

11
Nuclear aggregation of polyglutamine-expanded ataxin-3: fragments escape the cytoplasmic quality control.
2010-01-11

Expansion of a polymorphic polyglutamine segment is the common denominator of neurodegenerative polyglutamine diseases. The expanded proteins typically accumulate in large intranuclear inclusions and induce neurodegeneration. However, the mechanisms that determine the subcellular site and rate of inclusion formation are largely unknown. We found that the conserved putative ...

PubMed

12
Nuclear Aggregation of Polyglutamine-expanded Ataxin-3
2010-02-26

Expansion of a polymorphic polyglutamine segment is the common denominator of neurodegenerative polyglutamine diseases. The expanded proteins typically accumulate in large intranuclear inclusions and induce neurodegeneration. However, the mechanisms that determine the subcellular site and rate of inclusion formation are largely unknown. We found that the conserved putative ...

PubMed Central

13
FOXO3a is broadly neuroprotective in vitro and in vivo against insults implicated in motor neuron diseases
2009-06-24

Aging is a risk factor for the development of adult-onset neuro-degenerative diseases. While some of the molecular pathways regulating longevity and stress resistance in lower organisms are defined (i.e., those activating the transcriptional regulators DAF-16 and HSF-1 in C. elegans), their relevance to mammals and disease susceptibility are unknown. We studied the signaling controlled by the ...

PubMed Central

14
Antioxidants can inhibit basal autophagy and enhance neurodegeneration in models of polyglutamine disease.
2010-06-21

Many neurodegenerative diseases exhibit protein accumulation and increased oxidative stress. Therapeutic strategies include clearing aggregate-prone proteins by enhancing autophagy or decreasing oxidative stress with antioxidants. Many autophagy-inducing stimuli increase reactive oxygen species (ROS), raising concerns that the benefits of autophagy up-regulation may be counterbalanced by ROS ...

PubMed

15
Antioxidants can inhibit basal autophagy and enhance neurodegeneration in models of polyglutamine disease
2010-09-01

Many neurodegenerative diseases exhibit protein accumulation and increased oxidative stress. Therapeutic strategies include clearing aggregate-prone proteins by enhancing autophagy or decreasing oxidative stress with antioxidants. Many autophagy-inducing stimuli increase reactive oxygen species (ROS), raising concerns that the benefits of autophagy up-regulation may be counterbalanced by ROS ...

PubMed Central

16
Sodium selenate mitigates tau pathology, neurodegeneration, and functional deficits in Alzheimer's disease models.
2010-07-19

Alzheimer's disease (AD) brains are characterized by amyloid-beta-containing plaques and hyperphosphorylated tau-containing neurofibrillary tangles (NFTs); however, in frontotemporal dementia, the tau pathology manifests in the absence of overt amyloid-beta plaques. Therapeutic strategies so far have primarily been targeting amyloid-beta, although those targeting tau are only slowly beginning to ...

PubMed

17
Sodium selenate mitigates tau pathology, neurodegeneration, and functional deficits in Alzheimer's disease models
2010-07-19

Alzheimer's disease (AD) brains are characterized by amyloid-?-containing plaques and hyperphosphorylated tau-containing neurofibrillary tangles (NFTs); however, in frontotemporal dementia, the tau pathology manifests in the absence of overt amyloid-? plaques. Therapeutic strategies so far have primarily been targeting amyloid-?, although those targeting tau are only slowly beginning to emerge. ...

PubMed Central

18
Inhalation of Environmental Stressors & Chronic Inflammation: Autoimmunity and Neurodegeneration
2008-10-11

Human life expectancy and welfare has decreased because of the increase in environmental stressors in the air. An environmental stressor is a natural or human-made component present in our environment that upon reaching an organic system produces a coordinated response. This response usually involves a modification of the metabolism and physiology of the system. Inhaled environmental stressors ...

PubMed Central

19
Should the United States Abrogate Sovereignty Rights in the ...
1974-10-22

... Title : Should the United States Abrogate Sovereignty Rights in the Panama Canal Zone. Descriptive Note : Student essay,. ...

DTIC Science & Technology

20
Immune Dysfunctions and Abrogation of the Inflammatory ...
1981-08-01

... Title : Immune Dysfunctions and Abrogation of the Inflammatory Response by ... studies with UDMH in the mixed lymphocyte reaction (MLR) assay ...

DTIC Science & Technology

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