Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report the case of a 74 year old woman admitted to hospital for severe hypertension with unilateral renal artery thrombosis. Recanalisation of the renal artery was obtained by transluminal angioplasty leading to rapid control of the hypertension. Dynamic renal scintigraphy with MAG 3 confirmed the viability of the kidney distal to the thrombosis and, secondarily, the functional recovery of the affected kidney.
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PMID:[Renovascular hypertension due to renal artery thrombosis]. 974 30

Adult mammalian axon regeneration is generally successful in the peripheral nervous system (PNS) but is dismally poor in the central nervous system (CNS). However, many classes of CNS axons can extend for long distances in peripheral nerve grafts. A comparison of myelin from the CNS and the PNS has revealed that CNS white matter is selectively inhibitory for axonal outgrowth. Several components of CNS white matter, NI35, NI250(Nogo) and MAG, that have inhibitory activity for axon extension have been described. The IN-1 antibody, which recognizes NI35 and NI250(Nogo), allows moderate degrees of axonal regeneration and functional recovery after spinal cord injury. Here we identify Nogo as a member of the Reticulon family, Reticulon 4-A. Nogo is expressed by oligodendrocytes but not by Schwann cells, and associates primarily with the endoplasmic reticulum. A 66-residue lumenal/extracellular domain inhibits axonal extension and collapses dorsal root ganglion growth cones. In contrast to Nogo, Reticulon 1 and 3 are not expressed by oligodendrocytes, and the 66-residue lumenal/extracellular domains from Reticulon 1, 2 and 3 do not inhibit axonal regeneration. These data provide a molecular basis to assess the contribution of Nogo to the failure of axonal regeneration in the adult CNS.
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PMID:Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein. 1066 97

Three different myelin proteins, Nogo, MAG, and OMgp, inhibit regenerating axons after CNS injury. New work reveals that they all share a common receptor and that blockade of this receptor promotes CNS repair and functional recovery.
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PMID:Nerve regeneration: regrowth stumped by shared receptor. 1236 84

In vitro assays have shown that adult CNS tissue, in particular oligodendrocytes and myelin, contains several molecular constituents (Nogo-A/NI-220, MAG, several proteoglycans) which exert neurite growth inhibitory activity. Elimination of oligodendrocytes or myelin, or application of antibodies against some of these constituents enhance regenerative growth and compensatory sprouting of lesioned and unlesioned fiber tracts in spinal cord and brain. Enhanced growth is paralleled by various degrees of functional recovery.
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PMID:Increasing plasticity and functional recovery of the lesioned spinal cord. 1244 Mar 77

Investigations into the genetic basis of neuronal damage following spinal cord injury have thus far been limited to the acute phase after the injury. Using microarray analysis, the present study compared the spinal-cord-injury-induced gene expression changes in adult rats at the epicenter and rostral segments of spinal cord at acute (12 h) and delayed (42 days) time points. We have previously reported that the acute response to spinal cord injury involves alterations in genes responsible for inflammation, cell cycle alteration, and altered receptor function. In contrast, the delayed response includes changes in the expression of HSP27, MAG, MAP-2, IGF-1 and ApoE. The alteration in expression of these genes suggests an ongoing repair process in animals whose functional recovery has reached a plateau.
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PMID:Molecular evidence of repair and plasticity following spinal cord injury. 1507 26

Myelin-associated glycoprotein (MAG, Siglec-4) is one of several endogenous axon regeneration inhibitors that limit recovery from central nervous system injury and disease. Molecules that block such inhibitors may enhance axon regeneration and functional recovery. MAG, a member of the Siglec family of sialic acid-binding lectins, binds to sialoglycoconjugates on axons and particularly to gangliosides GD1a and GT1b, which may mediate some of the inhibitory effects of MAG. In a prior study, we identified potent monovalent sialoside inhibitors of MAG using a novel screening platform. In the current study, the most potent of these were tested for their ability to reverse MAG-mediated inhibition of axon outgrowth from rat cerebellar granule neurons in vitro. Monovalent sialoglycans enhanced axon regeneration in proportion to their MAG binding affinities. The most potent glycoside was disialyl T antigen (NeuAcalpha2-3Galbeta1-3[NeuAcalpha2-6]GalNAc-R), followed by 3-sialyl T antigen (NeuAcalpha2-3Galbeta1-3GalNAc-R), structures expressed on O-linked glycoproteins as well as on gangliosides. Prior studies indicated that blocking gangliosides reversed MAG inhibition. In the current study, blocking O-linked glycoprotein sialylation with benzyl-alpha-GalNAc had no effect. The ability to reverse MAG inhibition with monovalent glycosides encourages further exploration of glycans and glycan mimetics as blockers of MAG-mediated axon outgrowth inhibition.
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PMID:Potent glycan inhibitors of myelin-associated glycoprotein enhance axon outgrowth in vitro. 1570 48

Monocular deprivation normally alters ocular dominance in the visual cortex only during a postnatal critical period (20 to 32 days postnatal in mice). We find that mutations in the Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity. In NgR-/- mice, plasticity during the critical period is normal, but it continues abnormally such that ocular dominance at 45 or 120 days postnatal is subject to the same plasticity as at juvenile ages. Thus, physiological NgR signaling from myelin-derived Nogo, MAG, and OMgp consolidates the neural circuitry established during experience-dependent plasticity. After pathological trauma, similar NgR signaling limits functional recovery and axonal regeneration.
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PMID:Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor. 1619 31

NgR is a common receptor for three myelin-associated inhibitors and mediates their inhibitory activities on neurite outgrowth. In the present study, we investigated whether a DNA vaccine targeting NgR could play a beneficial role in improving recovery from spinal cord injury (SCI). We demonstrated that a DNA vaccine against NgR was successfully constructed and expressed efficiently in vitro and in vivo. After immunization with anti-NgR DNA vaccine, a low level of antibody response and a T cell-mediated immune response were induced in the vaccinated rats. And the antisera taken from the anti-NgR DNA vaccinated rats could partly reverse the inhibition of MAG on neurite outgrowth. When the rats were subjected to a contusive SCI, the vaccinated rats showed much better functional recovery than the controls. In those vaccinated rats that induced a T cell response and generated antibodies against NgR, functional improvements were even better. Histological assessments by three-dimensional reconstruction further demonstrated that the total lesion volume in the vaccinated rats was reduced by 30.8% compared to the controls. These results collectively suggest that DNA vaccine against NgR can significantly improve functional recovery in rats that received contusive SCI and that the vaccination approach may provide a promising strategy for promoting SCI repair.
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PMID:DNA vaccine against NgR promotes functional recovery after spinal cord injury in adult rats. 1736 86

Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are only recently coming to light. Potential mechanisms include changes in brain plasticity-promoting factors, unregulated expression of neurotoxic factors, or differences in the generation of scar tissue that impedes the formation of new axons and blood vessels in the infarcted region. Behaviorally, aged rats are more severely impaired by stroke than are young rats, and they also show diminished functional recovery. Infarct volume does not differ significantly in young and aged animals, but critical differences are apparent in the cytological response to stroke, most notably an age-related acceleration of the establishment of the glial scar. The early infarct in older rats is associated with a premature accumulation of BrdU-positive microglia and astrocytes, persistence of activated oligodendrocytes, a high incidence of neuronal degeneration, and accelerated apoptosis. Regeneration-associated mechanisms in the rat brain are active throughout life, albeit at lower levels in the aged animals. However; after stroke in aged rats, neuroepithelial marker-positive cells emanating largely from capillaries did not make a significant contribution to neurogenesis in the infarcted cortex of aged animals. Furthermore, the expression of plasticity-associated proteins, such as MAP1B, was delayed in aged rats. Tissue recovery was further delayed by the upregulation of Nogo, ephrin-A5 and MAG, which exert a powerful negative effect on axonal sprouting in the aged peri-infarct cortex, and by an age-related increase in the amount of the neurotoxic C-terminal fragment of the beta-amyloid precursor protein (betaAPP) at 2 wks post-stroke. Our findings indicate that the aged brain has the capability to mount a cytoproliferative response to injury, but the timing of the cellular and genetic response to cerebral insult is dysregulated in aged animals, thereby further compromising functional recovery. Elucidating the molecular basis of this phenomenon in the aging brain could yield novel approaches to neurorestoration following stroke or head injury in the elderly.
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PMID:The response of the aged brain to stroke: too much, too soon? 1769 75

Stress-promoting system is known to be involved in course and outcome of acute stage of ischemic stroke. An important predictor of an unfavorable course of stroke is so-called "low T3-syndrome". Therapy with drugs increasing T3 level on the background of reduced reaction of oxidative stress is one of a perspective direction of neuroprotection. The study aimed at investigating thyroliberin influence on a clinical course and an outcome of ischemic atherothrombotic stroke as well as on thyroid hormones level in 46 patients (27 women and 19 men) aged 55-75 years admitted to the hospital at the first 24 hours of the disease. Twenty-one patients were switched to thyroliberin in dosage 500 mcg twice a day during 5 days. A control group included 25 patients. Neurological status of the patients was evaluated on days 1, 3, 7 and 21 using the Orgogozo scale and functional recovery was assessed on day 21 with the Bartel scale. Radioimmunoassay of TTH level, cT3 and free thyroxine (cT4) in blood plasma was conducted on days 1, 2, 3 and 7 using test-kit IRMA TTG CT (Belorus). Atherosclerotic changes of MAG were measured with USDG on day 1. All the patients underwent MRI of the brain on days 1, 7 and 21 using tomograph Ellips (Russia) 0.15 Tesla. The dynamics of regress of neurological disturbances in patients receiving thyroliberin appeared as the higher total score on the Orgogozo scale on days 3, 7 and 21 especially in a severe course of the diseases compared to the control group (p<0,007 on day 7). The T3 level in these patients was significantly higher (p<0,05) on days 2, 3 and 7 and the thyroxine level was increased significantly on the 3rd day of stroke (p<0,005) as compared to the control group. In patients with moderate severity of the disease, the TTH level was significantly higher on the 2nd day of stroke (p=0,0004). However, in patients with a severe course TTH and T4 concentrations did not differ in both groups. The results of the study suggest that the use of thyroliberin in an acute stage of ischemic stroke prevents development of "low T3 syndrome" that promotes more rapid and essential regress of neurological disturbances.
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PMID:[Clinical and immunobiochemical study of efficacy and stress-protective properties of thyroliberin at the acute stage of carotid ischemic stroke]. 1819 36


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