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Biomedical subjects

C Hyman

Publications and source records attributed to C Hyman.

At least 19 recordsLinked to original sources
PubMed1999

Cerebral vasculopathy in sickle cell anemia: diagnostic contribution of positron emission tomography.

Children with sickle cell anemia (SS) have an increased risk for cerebral vasculopathy with stroke (CVA) and cognitive impairment. The present study examines the extent to which adding positron emission tomography (PET) to magnetic resonance imaging (MRI) can improve the detection of cerebral vasculopathy. Whereas MRI has been the prime modality for showing anatomical lesions, PET excels at assessing the functional metabolic state through glucose utilization 2-deoxy-2 [18F] fluoro-D-glucose (FDG) and microvascular blood flow ([15O]H2O). Forty-nine SS children were studied. Among them, 19 had clinically overt CVA, 20 had life-threatening hypoxic episodes or soft neurologic signs, and 10 were normal based on neurological history and examination. For the entire sample of 49 subjects, 30 (61%) had abnormal MRI findings, 36 (73%) had abnormal PET findings, and 44 (90%) showed abnormalities on either the MRI or the PET or both. Of the 19 subjects with overt CVA, 17 had abnormal MRI (89%), 17 had abnormal PET (89%), and 19 (100%) had either abnormal MRI or PET or both. Among the 20 subjects with soft neurologic signs, 10 (50%) had abnormal MRI, 13 (65%) had abnormal PET, and 17 (85%) had abnormal MRI and/or PET. Six (60%) of the 10 neurologically normal subjects had abnormal PET. Among the 30 subjects with no overt CVA, 25 (83%) demonstrated imaging abnormalities based on either MRI or PET or both, thus, silent ischemia. Lower than average full-scale intelligence quotient (FSIQ) was associated with either overt CVA or silent ischemic lesions. Four subjects who received chronic red blood cell transfusion showed improved metabolic and perfusion status on repeat PET scans. In conclusion, (1) the addition of PET to MRI identified a much greater proportion of SS children with neuroimaging abnormalities, particularly in those who had no history of overt neurologic events. (2) PET lesions are more extensive, often bihemispheric, as compared with MRI abnormalities. (3) PET may be useful in management as a tool to evaluate metabolic improvement after therapeutic interventions, and (4) the correlation of PET abnormalities to subsequent stroke or progressive neurologic dysfunction requires further study.

Adolescent↗
PubMed1999

Motherhood during the teen years: a developmental perspective on risk factors for childbearing.

The role of peer relations in childhood and behavioral and family characteristics in early adolescence as risk factors for adolescent childbearing was investigated. Sociometric surveys across third, fourth, and fifth grade and parent and child measures of behavioral and family functioning at sixth and eighth grade were collected in a lower income, urban sample of 308 African American females. Results replicated earlier findings on the role of childhood aggression as a predictor of teen motherhood. In addition, girls who displayed stable patterns of childhood aggression were at significantly higher risk not only to have children as teenagers but to have more children and to have children at younger ages. Results also indicated that females who were depressed in midadolescence were at greater risk to become parents between age 15 and 19 years. These findings demonstrate the need to take a differentiated approach to understanding teen childbearing and varying developmental pathways in the prediction of teen motherhood.

Adolescent↗
PubMed1998

Comorbidity of conduct and depressive problems at sixth grade: substance use outcomes across adolescence.

The comorbidity of conduct and depressive problems and substance use outcomes were examined in a community-based sample of 340 African American males and females. Alcohol, tobacco, and marijuana use were examined at Grades 6, 8, and 10 based on the following group membership at sixth grade: (a) comorbid conduct and depressive problems; (b) conduct problems only; (c) depressive problems only; (d) neither conduct nor depressive problems. Overall, the two conduct problem groups displayed the highest levels of substance use, although at some time points, comorbid youth displayed significant higher substance use levels. Subjects with depressive problems only displayed levels of substance use that were equivalent to subjects in the nonproblem group. Results highlight the importance of controlling for comorbid symptoms, possible interactive effects between conduct and depressive problems, and implications for treatment and prevention of substance use.

Adolescent↗
PubMed1996

A continuous striatal infusion of 6-hydroxydopamine produces a terminal axotomy and delayed behavioral effects.

Rat models of Parkinson's disease typically employ a rapid nigral injection of 6-hydroxydopamine (6-OHDA) to produce a near-complete loss of nigrostriatal dopamine neurons, and thus, model end stage disease. The present report describes the use of a continuous, low dose infusion of 6-OHDA into the striatum which produces a terminal axotomy of nigrostriatal dopamine neurons and protracted behavioral response. A solution of 6-OHDA in 0.4% ascorbate, delivered at 37 degrees C from osmotic minipumps, was stable for 8 days as determined by its retained toxicity to a dopaminergic neuroblastoma cell line. The continuous infusion of 0.2 mu g 6-OHDA per h did not affect the striatal uptake of [3H]%GABA, [3H]choline, or [3H]glutamate but reduced [3H]dopamine uptake by 55% within 1.5 days after the start of the infusion. The striatal infusion of 6-OHDA produced a dose-dependent reduction of striatal dopamine and DOPAC levels but did not alter HVA, 5-HT, or 5-HIAA. An increase in amphetamine-induced ipsiversive rotations occurred within 1.5 days after the acute striatal injection of 20 mu g or 30 mu g of 6-OHDA but required 4 days to develop with the continuous 6-OHDA infusion. The topography of the lesion mapped by [3H]mazindol binding showed that, beginning by 1.5 days, a diffuse depletion of terminals encompassed much of the striatum in the 30 mu g acute injection group, whereas in the continuously infused rats, the lesion was apparent only by 4 days and was restricted to a smaller and more completely lesioned area. Unlike acutely lesioned animals, continuously infused rats revealed no obvious loss of dopamine neurons in the pars compacta by 5 weeks after 6-OHDA. The continuous striatal infusion of 6-OHDA can produce a topographically limited terminal axotomy of dopamine neurons and a protracted behavioral impairment.

Animals↗
PubMed1996

Effects of donor age and brain-derived neurotrophic factor on the survival of dopaminergic neurons and axonal growth in postnatal rat nigrostriatal cocultures.

Early postnatal rat brain tissue can be grown for several weeks as organotypic slice cultures by the roller-tube method. We have here used this method to study the effects of donor age and brain-derived neurotrophic factor (BDNF) on the survival and growth of tyrosine hydroxylase immunoreactive (TH-i), dopaminergic (DA) neurons during the postnatal period when their nerve fibers normally innervate the striatal target. Tissue slices of ventral mesencephalon (VM) and striatum were prepared from newborn and 7-day-old rats and cocultured for 3--3 1/2 weeks with different combinations of the two donor ages. After immunocytochemical staining the number of TH-i, ventral mesencephalic neurons were counted, and the growth of TH-i fibers into the striatal part of the cocultures was evaluated. Co-cultures, with both VM and striatal slices prepared from newborn rats, contained a significantly higher number of TH-i neurons and displayed a significantly increased innervation of the striatal slices compared with other combinations of donor ages. Addition of BDNF resulted in both an increased survival of TH-i neurons and an increased growth of TH-i fibers into the cocultured striatal slices. Significant neurotrophic effect of BDNF did, however, require young donor age of both VM and striatal slices. It is suggested that BDNF induces more cells, possibly progenitor cells, to express TH immunoreactivity. Alternatively BDNF may suppress apoptotic cell death documented by others to occur in the postnatal rat substantia nigra pars compacta. Irrespective of the mechanisms, survival of more TH-i neurons was related to an increased innervation of the striatal slices by TH-i nerve fibers. The observed effects of BDNF on both survival and fiber growth of TH-i neurons indicate a potential role of BDNF for treatment of Parkinson's disease or grafts of immature DA neurons transplanted to patients with Parkinson's disease. A significant trophic effect of BDNF did, however, seem to depend on young developmental age of both striatum and VM. Parallel treatment with striatal neurotrophic factors may therefore be a necessary prerequisite to a trophic effect of BDNF under clinical conditions.

Age Factors↗
PubMed1995

Comparison of the effects of the neurotrophins on the morphological structure of dopaminergic neurons in cultures of rat substantia nigra.

The effect of the various neurotrophin family members on the morphological structure of dopaminergic neurons was compared in dissociated cultures of embryonic rat ventral mesencephalon. Cultures were maintained in vitro in the presence of brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrohin-4/5 (NT-4/5), nerve growth factor (NGF) or no added growth factors. Three-dimensional reconstructions of 48 neurons were made in each of the experimental groups following immunocytochemical staining for tyrosine hydroxylase to detect dopaminergic neurons. In addition [3H]mazindol binding analyses were carried out in replicate cultures in order to quantify the effects of the neurotrophins on the number of dopamine uptake sites. Among the neurotrophins tested, NT-4/5 influenced the proximal morphological parameters most, as determined by a 36% increase in the soma profile area and 35% in the number of stem neurites. Analysis of neuritic size and complexity in these cultures revealed that combined neuritic length and number of segments/cell were increased by 45 and 40% respectively. A change in neurite complexity in the NT-4/5 treated cultures was further confirmed using Scholl's concentric sphere analysis. In addition, relative to the control, NT-4/5 increased the neuronal differentiation as evidenced by increases in varicosity density and [3H]mazindol binding by 114 and 101% respectively. BDNF and, to a lesser extent, NT-3 also increased both proximal parameters and parameters of differentiation, but were without effect on parameters of neuritic size and complexity. No effects on neuronal structure were observed in NGF treated cultures. These findings demonstrate that BDNF, NT-3 and NT-4/5 influence the morphological differentiation of dopaminergic neurons in vitro, suggesting they may play a role in the structural development and plasticity of these neurons in the mesencephalon.

Animals↗
PubMed1995

Effects of BDNF on dopaminergic, serotonergic, and GABAergic neurons in cultures of human fetal ventral mesencephalon.

The neurotrophin brain-derived neurotrophic factor (BDNF) was tested for its ability to promote the survival and regulation of expression of phenotypic markers of dopaminergic, serotonergic, and GABAergic neurons in free-floating roller tube cultures of human fetal ventral mesencephalon. This culture system contains neurons of the anlage of the substantia nigra as well as that of the rostral raphe nucleus. Dopaminergic neuron number and tyrosine hydroxylase (TH) fiber density was monitored by TH immunocytochemistry. Measurement of dopamine (DA) content, TH enzymatic activity, serotonin (5-HT) content, and glutamic acid decarboxylase (GAD) activity were used as indices of their respective neurotransmitter function. The presence of GABAergic and serotonergic neurons in this culture system was confirmed by GABA and 5-HT immunocytochemistry. In cultures maintained in the presence of BDNF (10 ng/ml), the density of TH-positive cells was increased by 2.5-fold (P F 0.05), and the TH-positive fiber density was increased by 3.5-fold (P F 0.01), relative to control cultures. Similarly, the relative increases in DA content and TH activity were 2.6- and 2.3-fold, respectively, in the BDNF-treated cultures (P F 0.01 and P F 0.01). On a per neuron basis, DA content and TH activity were not markedly changed by BDNF treatment, suggesting that the increases in DA content and TH activity are due to more DA neurons surviving. Relative elevations were also observed in serotonin content (2.0-fold, P F 0.01) and GAD enzymatic activity (1.4-fold, P F 0.01). Future studies will need to determine whether these changes result from the direct action of BDNF on these neurons or through some indirect mechanism. The results demonstrate that BDNF has beneficial effects on cultured human fetal tissue, which may be relevant in optimizing neuronal transplantation techniques, and that multiple systems are simultaneously influenced by BDNF.

Abortion, Induced↗
PubMed1994

The neurotrophins NT-4/5 and BDNF augment serotonin, dopamine, and GABAergic systems during behaviorally effective infusions to the substantia nigra.

Brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) have both been identified as ligands for the TrkB receptor, yet differences have emerged in terms of their in vitro potencies for neuronal survival and differentiation. This has prompted the in vivo study of their effects on behavior and neuro-chemical parameters associated with dopamine, serotonin, and GABAergic neurons in the basal ganglia. Two-week supranigral infusions of NT-4/5 and BDNF were similar in their ability to augment levels of the dopamine metabolite homovanilic acid (HVA) (63 and 78%, respectively) and the ratios of dihydroxphenylacetic acid/dopamine (DOPAC/DA) (39, 48%) and HVA/DA (85, 77%) in the caudate-putamen of the hemisphere ipsilateral to the nigral infusion. Striatal concentrations of DOPAC were elevated 45% by BDNF but not by NT-4/5. The 3-MT/dopamine ratio, an indicator of dopamine release, was elevated by 38 and 32% in the striata of BDNF- and NT-4/5-infused rats, respectively. Striatal indoleamine metabolism, determined by the ratio of 5-hydroxyindoleacetic acid (5HIAA)/serotonin was also elevated by NT-4/5 and BDNF in the caudate-putamen (29, 32%), and the 5HIAA content of the substantia nigra was elevated by both factors (43, 40%). The activity of GAD within the superior colliculus was elevated 21 and 41% by BDNF and NT-4/5, respectively. A contraversive rotational bias was induced in BDNF and NT-4/5-treated rats challenged with d-amphetamine, and these responses were blocked by pretreatment with selective D1 or D2 receptor antagonists but not by opiate receptor antagonism. Thus, NT-4/5 and BDNF can elevate the turnover of dopamine through both metabolic and release pools and augment the behavioral response to d-amphetamine. The role for dopamine in this behavioral response is indicated by the requirement of unoccupied D1 and D2 receptors, but may also involve changes in serotonergic, GABAergic, or other pathways. The TrkB receptor-specific actions of BDNF and NT-4/5 may have implications for understanding the etiology or treatment of basal ganglia disorders.

Animals↗
PubMed1994

Efficacy of brain-derived neurotrophic factor and neurotrophin-3 on neurochemical and behavioral deficits associated with partial nigrostriatal dopamine lesions.

Brain-derived neurotrophic factor (BDNF) promotes the survival of dopamine (DA) neurons, enhances expression of DA neuron characteristics, and protects these cells from 6-hydroxydopamine (6-OHDA) toxicity in vitro. We tested the ability of BDNF or neurotrophin-3 (NT-3) to exert similar protective effects in vivo during chronic delivery of 6-OHDA to the rat neostriatum. Chronic infusions of BDNF or NT-3 (12 micrograms/day) above the substantia nigra were started 6 days before and continued during an 8-day chronic intrastrial infusion of 6-OHDA. In control and neurotrophin-treated animals, 6-OHDA treatment selectively depleted 50-60% of nigrostriatal DA nerve terminals but produced little if any loss of pars compacta DA cell bodies. This partial DA lesion resulted in three rotations per minute toward the lesioned hemisphere after treatment with the DA release-inducing drug d-amphetamine. Compared with supranigral infusions of vehicle, BDNF and NT-3 decreased the number of these ipsiversive rotations by 70 and 48% and increased by 20- and 10-fold, respectively, the number of contraversive rotations observed after amphetamine injection. When challenged with the DA receptor agonist apomorphine, BDNF- and NT-3-treated animals also exhibited a seven- and 3.5-fold increase in the number of contraversive rotations relative to the vehicle group, respectively. Compared with vehicle, BDNF increased striatal levels of homovanillic acid (HVA; 86%), 3,4-dihydroxyphenylacetic acid (DOPAC; 42%), and 5-hydroxyindoleacetic acid (5-HIAA; 32%) and the HVA/DA (43%) and 5-HIAA/serotonin (34%) ratios in the DA-denervated striatum. NT-3 augmented only striatal 5-HIAA levels (24%). Neither factor altered the 6-OHDA-induced decrease in striatal DA levels or high-affinity DA uptake and thus did not protect against the destruction of DA terminals and did not alter striatal D1 or D2 ligand binding. Choline, GABA, and glutamate uptake in the striatum were not altered by the lesion or neurotrophin treatment. Thus, BDNF and to a lesser extent NT-3 reverse rotational behavioral deficits and augment striatal DA and 5-HT metabolism in a partial DA lesion model.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Overlapping and distinct actions of the neurotrophins BDNF, NT-3, and NT-4/5 on cultured dopaminergic and GABAergic neurons of the ventral mesencephalon.

The neurotrophins brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5) were compared for their effects in promoting the survival and/or regulation of expression of phenotypic markers of dopaminergic and GABAergic neurons in cultures derived from embryonic rat ventral mesencephalon. Dopaminergic neuron number and phenotypic expression were monitored by tyrosine hydroxylase (TH) immunocytochemistry, and measurement of high-affinity dopamine uptake activity and dopamine content, respectively. High-affinity GABA uptake, glutamic acid decarboxylase (GAD) activity, and endogenous GABA content were used to detect GABAergic neurons. Seven days of treatment with either BDNF or NT-3 resulted in dose-dependent increases in the number of TH-positive neurons, with maximal responses of 3-fold and 2.3-fold, respectively. Dopamine uptake activity and dopamine content were similarly increased. The effects of BDNF and NT-3 on dopamine uptake activity showed no additivity. NT-4/5 treatment elicited the greatest increase (7-fold) in the number of TH-positive neurons, as well as a 2.6-fold increase in dopamine content. In marked contrast to BDNF or NT-3, NT-4/5 had no effect on dopamine uptake capacity. BDNF, NT-3, or NT-4/5 also produced dose-dependent elevations of 2-3-fold in GABA uptake activity. These effects were not additive. GAD activity was increased by BDNF (1.8-fold) and NT-3 (threefold) treatment, but not by NT-4/5, whereas GABA content was increased to a similar extent by all three neurotrophins. NGF had no effect on any of the parameters measured in this study. Northern analyses indicated that the mRNAs encoding TrkB and TrkC, the functional high-affinity receptors for BDNF and NT-4/5, and NT-3, respectively, are expressed in the substantia nigra of adult rat brain, as well as in cultures of developing ventral mesencephalon. Taken together, our results indicate that BDNF and NT-3 have broadly similar effects in promoting the survival and differentiated phenotype of both dopaminergic and GABAergic neurons of the developing substantia nigra. Although BDNF and NT-4/5 are thought to act through the same high-affinity receptor, TrkB, it is evident that these two neurotrophins have distinct as well as overlapping actions toward mesencephalic dopaminergic or GABAergic neurons.

Animals↗
PubMed1993

The therapeutic potential of neurotrophic factors in the treatment of Parkinson's disease.

Partial symptomatic relief from Parkinson's disease with levodopa has proven to be one of the rare success stories in the development of drugs to combat neurodegenerative diseases. However, no therapeutic agent has yet conclusively been shown to slow, halt, or reverse the underlying progression of neuronal loss in Parkinson's disease or any other human neurodegenerative disorder. This article reviews recent developments in the biology of neurotrophic growth factors, especially members of the nerve growth factor-related neurotrophin family, which may point to their potential as therapeutic agents for the treatment of Parkinson's disease. Parkinson's disease, characterized by the progressive loss of dopaminergic neurons of the substantia nigra, is one of the most well-characterized neurodegenerative disorders from both an anatomical and biochemical standpoint, but as yet the etiology of this disease remains poorly understood. Epidemiological, neurochemical, and pathological studies have provided a wealth of data that have spawned many theories of the underlying cause of Parkinson's disease, including environmental and genetic origins. Future elucidation of the disease process in Parkinson's disease may yield obvious therapeutic strategies, but even in the absence of such knowledge there are several general approaches that can be taken as strategies for the treatment of a "focal" neurodegenerative disease. These include: (a) mimetics, activation of the postsynaptic target(s) of the missing neurons through mimetics of the missing neurotransmitter, e.g., use of a dopamine precursor or dopamine receptor agonist in Parkinson's disease; (b) transplants, replenishment of the missing neurons via transplantation of neurons or nonneuronal cells secreting the appropriate neurotransmitter, e.g., fetal nigral grafts in Parkinson's disease; (c) neurotrophic factors or neuroprotectants, intervention with neurotrophic factors/neuroprotective agents which slow, halt, or reverse the progression of neuronal degeneration, e.g., a dopamine neurotrophic factor in Parkinson's disease. The scope of the present article is limited to a review of recent progress in the biology of neurotrophic factors that relates to their potential clinical use in treating the loss of dopamine neurons in Parkinson's disease.

Animals↗
PubMed1992

Brain-derived neurotrophic factor augments rotational behavior and nigrostriatal dopamine turnover in vivo.

Brain-derived neurotrophic factor (BDNF), a member of the nerve growth factor (NGF)-related family of neutrophins, promotes the survival and differentiation of cultured nigral dopamine neurons. Two-week infusions of BDNF were made above the right pars compacta of the substantia nigra in adult rats. Systemic injection of these animals with (+)-amphetamine, a dopamine-releasing drug, induced 3 or 4 body rotations per minute directed away from the nigral infusion site. Neither supranigral NGF nor neocortical BDNF infusions induced rotational behavior. Systemic injections of the postsynaptic dopamine receptor agonist apomorphine did not induce rotations in these animals, demonstrating a presynaptic dopamine neuron locus for BDNF action. In support of this, neostriatal levels of the dopamine metabolite homovanillic acid (HVA) were elevated by 28%, and the HVA/dopamine and dihydroxyphenylacetic acid (DOPAC)/dopamine ratios were elevated by 56% and 34%, respectively, in the BDNF-infused brain hemisphere. BDNF augmented striatal concentrations of HVA and DOPAC and the metabolite/dopamine ratios to even greater extents after (+)-amphetamine injection, when peak rotational effects occurred. Intrastriatal infusions of BDNF produced fewer rotations per minute (1-2.5) after (+)-amphetamine and smaller elevations in HVA and the HVA/dopamine ratio (15% and 30%, respectively) than after supranigral delivery. Neither striatal dopamine, gamma-aminobutyric acid, nor acetylcholine high-affinity uptake or the synthetic enzymes for these neurotransmitters was altered by BDNF. These behavioral and neurochemical effects demonstrate an action of BDNF on dopamine neurons in vivo and are consistent with a potential role for BDNF in the treatment of Parkinson disease.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Predicting early adolescent disorder from childhood aggression and peer rejection.

Two large cohorts of Black 3rd-grade children from low-income families were followed into early adolescence. Adjustment at the end of the 1st year of middle school was assessed by teacher and parent ratings and by adolescent self-reports. Childhood peer social status predicted parent-reported externalized and internalized disorder and self-reported internalized disorder. Childhood aggression predicted self-reported externalized and internalized disorder and parent-reported externalized disorder. Teacher ratings of school adjustment were predicted by aggression, rejection, and sex of the child. Consensus judgments of poor adjustment were predicted by both aggression and peer rejection, with sex moderating the effect of peer rejection. Both childhood aggression and peer rejection appear to be significant predictors of adolescent disorder, with each making a predictive contribution uniquely its own.

Adolescent↗
PubMed1992

Brain-derived neurotrophic factor protects dopamine neurons against 6-hydroxydopamine and N-methyl-4-phenylpyridinium ion toxicity: involvement of the glutathione system.

Brain-derived neurotrophic factor (BDNF) has recently been shown to enhance the survival of dopamine neurons in cultures derived from the embryonic rat mesencephalon. We now extend this study by demonstrating that, in addition to the effect of sustaining survival of dopaminergic neurons, BDNF also confers protection against the neurotoxic effects of 6-hydroxydopamine (6-OHDA) and N-methyl-4-phenylpyridinium ion (MPP+). Exposure of mesencephalic cultures to either 6-OHDA or MPP+ resulted in a loss of 70-80% of dopaminergic neurons, as determined by tyrosine hydroxylase (TH) immunocytochemistry. In BDNF-treated cultures, loss of TH-positive cells after exposure to either toxin was reduced to only 30%. To facilitate biochemical measurements, we studied SH-SY5Y dopaminergic neuroblastoma cells. BDNF was found to protect these cells from the dopaminergic neurotoxins, 6-OHDA and MPP+. Indicative of oxidative stress, treatment of SH-SY5Y cells with 10 microM 6-OHDA for 24 h caused a fivefold increase in the levels of oxidized glutathione (GSSG). Pretreatment with BDNF for 24 h completely prevented the rise in GSSG. Further examination revealed that BDNF increased the activity of the protective enzyme, glutathione reductase, by 100%. In contrast, BDNF had no effect on the activity of catalase. These results add further impetus to exploring the therapeutic potential of BDNF in animal models of Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1991

BDNF is a neurotrophic factor for dopaminergic neurons of the substantia nigra.

Brain-derived neurotrophic factor (BDNF), present in minute amounts in the adult central nervous system, is a member of the nerve growth factor (NGF) family, which includes neurotrophin-3 (NT-3). NGF, BDNF and NT-3 all support survival of subpopulations of neural crest-derived sensory neurons; most sympathetic neurons are responsive to NGF, but not to BDNF; NT-3 and BDNF, but not NGF, promote survival of sensory neurons of the nodose ganglion. BDNF, but not NGF, supports the survival of cultured retinal ganglion cells but both NGF and BDNF promote the survival of septal cholinergic neurons in vitro. However, knowledge of their precise physiological role in development and maintenance of the nervous system neurons is still limited. The BDNF gene is expressed in many regions of the adult CNS, including the striatum. A protein partially purified from bovine striatum, a target of nigral dopaminergic neurons, with characteristics apparently similar to those of BDNF, can enhance the survival of dopaminergic neurons in mesencephalic cultures. BDNF seems to be a trophic factor for mesencephalic dopaminergic neurons, increasing their survival, including that of neuronal cells which degenerate in Parkinson's disease. Here we report the effects of BDNF on the survival of dopaminergic neurons of the developing substantia nigra.

Animals↗
PubMed1989

Nutritional impact of acquired immune deficiency syndrome: a unique counseling opportunity.

The acquired immune deficiency syndrome (AIDS) presents a challenge for dietitians. Changes in the immune system have a potentially detrimental effect on nutritional status as a result of conditions such as anorexia, infection, diarrhea, and drug side effects. Conversely, poor nutrition status may adversely alter the immune systems. Dietary guidelines for the management of these conditions and additional obstacles are discussed. When counseling patients with AIDS, the dietitian needs to be aware of and sensitive to alternative therapies, to evaluate their effectiveness, and to assist in determining their place in the patient's treatment. Psychosocial factors that could influence nutritional status, such as dementia, unemployment, and isolation, must also be taken into consideration. A nutrition program has been established to address the needs of AIDS patients at AIDS Project Los Angeles-Necessities of Life Program (APLA-NOLP), a food distribution center. The goal of the program is to maintain or improve the client's nutritional status by providing education and counseling. The nutrition program has been enthusiastically received, and the outcome of the program on the nutritional status of the participants is currently under study. The dietitian is in a unique position to intervene by providing resource information, food preparation tips, and individualized nutrition plans. It is imperative that the dietitian become familiar with the AIDS disease process and its implications for nutritional status to be considered an expert in the nutrition management of such patients.

Acquired Immunodeficiency Syndrome↗