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Hypersensitivity of DJ-1-deficient mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine (MPTP) and oxidative stress.
DJ-1 protects against neuronal oxidative stress, and loss of DJ-1 may lead to Parkinson's disease by conferring hypersensitivity to dopaminergic insults. Expand
Cyclin-dependent kinase 5 is a mediator of dopaminergic neuron loss in a mouse model of Parkinson's disease
It is proposed that cdk5 is a key regulator in the degeneration of dopaminergic neurons in Parkinson's disease after administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that damages the nigrostriatal dopamine pathway. Expand
Inhibition of Calpains Prevents Neuronal and Behavioral Deficits in an MPTP Mouse Model of Parkinson's Disease
Protection against nigral neuron degeneration in PD may be sufficient to facilitate normalized locomotor activity without necessitating striatal reinnervation, according to the results of a mouse model of PD. Expand
Involvement of interferon-gamma in microglial-mediated loss of dopaminergic neurons.
It is reported here that PD patients express significantly elevated levels of IFN-gamma in their blood plasma, and the interactions between microglia and dopaminergic neurons in an in vitro mixedMicroglia/midbrain neuron rotenone-induced death paradigm suggest that IFN -gamma participates in death of dopamine neurons by regulating microglial activity. Expand
The pathogenesis of clinical depression: Stressor- and cytokine-induced alterations of neuroplasticity
Depressive illness may be considered a disorder of neuroplasticity as well as one of neurochemical imbalances, and cytokines may act as mediators of both aspects of this illness. Expand
Neurotransmitter, peptide and cytokine processes in relation to depressive disorder: Comorbidity between depression and neurodegenerative disorders
The view is taken that synergy between stressors and inflammatory factors may promote pathological outcomes through their actions on neuropeptides and several neurotransmitters. Expand
Synergistic Effects of Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α: Central Monoamine, Corticosterone, and Behavioral Variations
The proinflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) influence neuroendocrine activity, promote central neurotransmitter alterations, and induce aExpand
Cytokines as a precipitant of depressive illness: animal and human studies.
It is proposed that chronic cytokine elevations engender neuroendocrine and brain neurotransmitter changes that are interpreted by the brain as being stressors, and contribute to the development of depression. Expand
Regulation of Dopaminergic Loss by Fas in a 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Model of Parkinson's Disease
Although critical for degeneration of the soma, Fas deficiency did not significantly prevent the reduction of dopaminergic terminal fibers within the striatum or normalize the activation of striatal microglia and elevation of the postsynaptic activity marker ΔFosB induced by denervation. Expand
Psychogenic, neurogenic, and systemic stressor effects on plasma corticosterone and behavior: mouse strain-dependent outcomes.
It appears that whereas stressor reactivity and adrenal glucocorticoid release may be exaggerated in BALB/cByJ mice, such effects may be dependent on the specific characteristic of the stressor situation. Expand