Disease relevance of Nerve Degeneration

• The identification of the M. leprae-targeted Schwann cell receptor, dystroglycan, and its associated molecules in myelination, demyelination and axonal functions suggests a role for these molecules in early nerve degeneration [1].
• To elucidate factors related to selective dopamine neuron degeneration in Parkinson's disease (PD), we have defined gene expression profiles of discrete dopamine neuron subpopulations in the rat using immunofluorescent laser capture microscopy and microarray analysis [2].
• OBJECTIVE: To define the role of the type 1 angiotensin II (AT1) and type II (AT2) receptors in the development of salt-sensitive hypertension induced by sensory nerve degeneration [3].
• Intracerebroventricular kainic acid administration in rat, a model of temporal lobe epilepsy, results in CA3 pyramidal neuron degeneration leading to deafferentation of CA1 pyramidal neurons [4].
• Estrogen modulates many features of the sympathetic nervous system, including cell numbers and ganglion synapses, and can induce uterine sympathetic nerve degeneration [5].

Psychiatry related information on Nerve Degeneration

• Peak response time to levodopa appears to reflect predominantly the status of compensatory presynaptic dopaminergic mechanisms and thus may provide an index to the degree of dopamine neuron degeneration in parkinsonian patients [6].
• Conversely, no hypocretin neuron degeneration has been observed in the genetic form of narcolepsy in dogs but no trace of hypocretin was seen in the brain or the CSF in cases of sporadic canine narcolepsy [7].

High impact information on Nerve Degeneration

• BAG5 inhibits parkin and enhances dopaminergic neuron degeneration [8].
• We provide evidence that the photoreceptor neuron degeneration seen in flies expressing mutant human huntingtin correlates with widespread degenerative events in the Drosophila CNS [9].
• The information on the position of the Wld locus should be valuable in further characterization of this gene involved in nerve degeneration and regeneration [10].
• Expression of apolipoprotein E during nerve degeneration and regeneration [11].
• The mechanism or mechanisms whereby PS-1 mutations promote neuron degeneration in AD are unknown [12].

Chemical compound and disease context of Nerve Degeneration

• In the present study, we tested the hypothesis that 17beta-estradiol (betaE2) is a neuroprotectant in the retina, using two experimental approaches: 1) hydrogen peroxide (H(2)O(2))-induced retinal neuron degeneration in vitro, and 2) light-induced photoreceptor degeneration in vivo [13].
• We demonstrated that both betaE2 and 17alpha-estradiol (alphaE2) significantly protected against H(2)O(2)-induced retinal neuron degeneration; however, progesterone had no effect. betaE2 transiently increased the phosphoinositide 3-kinase (PI3K) activity, when phosphoinositide 4,5-bisphosphate and [(32)gammaATP] were used as substrate [13].
• Because 6-hydroxydopamine (6-OHDA) is thought to induce nigrostriatal dopaminergic neuronal lesions via metal-catalyzed free radical formation, the effect of the iron chelator desferrioxamine was investigated on 6-OHDA-induced dopaminergic neuron degeneration in the rat [14].
• During the interval of nerve degeneration, there was a significant reduction of bromodeoxyuridine incorporation from 24 h of nerve injury (39 +/- 7% of the control side, p 0.01) [15].
• Reductions in muscimol binding to the gamma-aminobutyric acidA receptor had the closest relationship with neuron degeneration, whereas pirenzepine binding appeared to reflect a compensation in muscarinic receptors for changes in neuron densities [16].

Biological context of Nerve Degeneration

• The unique pattern of signaling pathways recruited by ET-1 and its combined effects on regulation of phenotype and proliferation of SC suggest an important role for this peptide during nerve degeneration/regeneration [17].
• The participation of iron-induced oxygen free radicals in the process of nigrostriatal dopamine neuron degeneration is strengthened by recent studies in which the neurotoxicity of 6-OHDA has been linked to the release of iron from its binding sites in ferritin [18].
• CONCLUSIONS: Nerve degeneration (i.e. MNFD) correlated with clinical neuropathy but not with glucose tolerance status whereas nerve myo-inositol levels positively correlated with signs of nerve regeneration (i.e. increased cluster density) [19].
• Riz maps to distal chromosome 4 near genes involved in tumorigenesis and nerve degeneration [20].
• In addition, during the retrograde neuron degeneration in SN, the level of heme oxygenase-1 immunopositivity, an oxidative stress marker, was markedly increased in SNpc neurons [21].

Anatomical context of Nerve Degeneration

• These data indicate that myelin phospholipids are completely hydrolyzed during nerve degeneration, that at least half the resultant free fatty acids are salvaged and reutilized for new myelin synthesis, and that these salvaged fatty acids are transported by a lipoprotein-mediated mechanism similar to that functioning in cholesterol reutilization [22].
• After bilateral ganglionectomy, the histamine level significantly increased in both hemi-dura 15-60 days post-surgery, whereas the serotonin level had significantly increased at 60 days post-surgery.These results clearly demonstrate, for the first time, a long-term trophic effect of sympathetic nerve degeneration on mast cells in the dura mater [23].
• Ca2+ dependence of the release of noradrenaline during nerve degeneration in the parotid gland [24].
• PPLA2 is a candidate gene for distal HMN II in this family since it is expressed in the peripheral nervous system during nerve degeneration [25].
• These results suggest that a selective COX-2 inhibitor is effective in the effector phase by its influence on macrophages that are responsible for nerve degeneration [26].

Gene context of Nerve Degeneration

• These results suggest that the mutation in Cct4 underlies cutaneous nerve degeneration in mf rats [27].
• Notably, alpha-tocopherol effectively prevented IFN-gamma/LPS-induced dopaminergic neuron degeneration, without affecting iNOS induction and nitric oxide production [28].
• Recently, it was demonstrated that CEP-1347/KT7515 attenuated MPTP-induced nigrostriatal dopaminergic neuron degeneration in mice, as well as MPTP-induced JNK phosphorylation [29].
• However, the relationship between abnormal aggregates of alpha-synuclein and human dopamine (DA) neuron degeneration remains unclear [30].
• We tested each of the neurotrophins BDNF, NT-3, NT-4/5 and NGF for their ability to support auditory neuron survival following a two-week period of deafness in guinea pigs, when approximately 15% auditory neuron degeneration has already occurred [31].

Analytical, diagnostic and therapeutic context of Nerve Degeneration

• These results support the view that progressive dopamine neuron degeneration reduces the brain's ability to buffer shifts in levodopa availability attending its periodic oral administration; the clinical result is wearing-off phenomenon [32].
• We investigated the microglial response to progressive dopamine neuron degeneration using in vivo positron emission tomography (PET) imaging and postmortem analyses in a Parkinson's disease (PD) rat model induced by unilateral (right side) intrastriatal administration of 6-hydroxydopamine (6-OHDA) [33].
• The time-course and extent of LC neuron degeneration were analyzed quantitatively in Nissl-stained sections, and the regenerative response of residual neurons was characterized by dopamine-beta-hydroxylase immunohistochemistry [34].
• While 6-hydroxydopamine (6-OHDA) is often used in animal models of DA neuron degeneration, there have been relatively few studies that have examined the effects of 6-OHDA in older animals [35].

References