Amyotrophic lateral sclerosis: changes of noradrenergic and serotonergic transmitter systems in the spinal cord

Bertel, O; Malessa, S.; Sluga, E; Hornykiewicz, Oleh

doi:10.1016/0006-8993(91)91680-y

Cited by 46 publications

(35 citation statements)

References 43 publications

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“…CSF concentrations of other amino acids, i.e., aspartate and glycine, did not significantly differ between ALS and controls (Niebroj-Dobosz et al 1999). Changes in the concentrations of serotonin and its metabolite, 5-hydroxyindoleacetic acid, were also reported in the spinal cord of ALS patients, but it is unknown whether CSF is able to reflect such alterations (Bertel et al 1991).…”

Section: Biomarkers Of the Neurotransmission In Csfmentioning

confidence: 95%

CSF markers in amyotrophic lateral sclerosis

et al. 2012

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Amyotrophic lateral sclerosis (ALS, 'Lou Gehrig disease') is the most common, progressive, neurodegenerative, motor neuron disease, causing damage to upper and lower motor neurons, leading to paralysis and death within 3-5 years. Majority of ALS cases are sporadic ALS (SALS) and only 5-10 % of cases are familial ALS (FALS). Pathogenesis of ALS is complicated and still unclear, including genetic, glutamate excitotoxicity, oxidative stress, mitochondrial dysfunction, neurofilament accumulation, impaired trophic support, altered glial function, viral infection, immune imbalance and impairment of the blood-brain, blood-spinal cord and blood-cerebrospinal fluid barriers (BBB/BSCB/BCSFB). The CSF analysis is still one of the basic laboratory tools and might reflect pathophysiological alterations in the course of the disease and could provide an insight into disease pathomechanisms. The most important aim of its analysis is evaluation of blood-CSF barrier, which is altered in 46 % of ALS patients. The CSF biomarkers may give insight into ALS pathophysiology and may be useful for early, presymptomatic diagnosis, therapeutic monitoring and the development of new therapeutic strategies. This review summarizes the general concepts of biomarkers in CSF of ALS patients and their potential usefulness in further research.

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Section: Biomarkers Of the Neurotransmission In Csfmentioning

confidence: 95%

CSF markers in amyotrophic lateral sclerosis

et al. 2012

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“…Bertel et al found norepinephrine concentrations in thoracic and lumbar spinal cord of amyotrophic lateral sclerosis patients 2-to 4-fold higher compared with values obtained in control patients [53]. Moreover, the elevation of plasma norepinephrine levels in amyotrophic lateral sclerosis patients may be related to progression of respiratory failure and lower motor neuron dysfunction.…”

Section: Amyotrophic Lateral Sclerosismentioning

confidence: 95%

Potential links between neurological disease and Tako-Tsubo cardiomyopathy: A literature review

Santoro

Carapelle

Ortiz

et al. 2013

International Journal of Cardiology

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“…These data have been reported in a detailed review by Sandyk (2006). As a whole, the data suggest that ALS patients have lower 5-HT levels because of a decrease in the production and/or release of 5-HT (Bertel et al 1991;Monaco et al 1979 Means Ϯ SD (n ϭ 20 per drug level) are presented for tremor onset, rotarod onset of decline, and end stage. Data are divided into drug levels (vehicle, 5 mg/kg, and 10 mg/kg).…”

Section: Discussionmentioning

confidence: 66%

Effect of fluoxetine on disease progression in a mouse model of ALS

Koschnitzky

Quinlan

Lukas

et al. 2014

Journal of Neurophysiology

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Koschnitzky JE, Quinlan KA, Lukas TJ, Kajtaz E, Kocevar EJ, Mayers WF, Siddique T, Heckman CJ. Effect of fluoxetine on disease progression in a mouse model of ALS. J Neurophysiol 111: 2164-2176, 2014. First published March 5, 2014 doi:10.1152/jn.00425.2013.-Selective serotonin reuptake inhibitors (SSRIs) and other antidepressants are often prescribed to amyotrophic lateral sclerosis (ALS) patients; however, the impact of these prescriptions on ALS disease progression has not been systematically tested. To determine whether SSRIs impact disease progression, fluoxetine (Prozac, 5 or 10 mg/kg) was administered to mutant superoxide dismutase 1 (SOD1) mice during one of three age ranges: neonatal [postnatal day (P)5-11], adult presymptomatic (P30 to end stage), and adult symptomatic (P70 to end stage). Long-term adult fluoxetine treatment (started at either P30 or P70 and continuing until end stage) had no significant effect on disease progression. In contrast, neonatal fluoxetine treatment (P5-11) had two effects. First, all animals (mutant SOD1 G93A and control: nontransgenic and SOD1 WT ) receiving the highest dose (10 mg/kg) had a sustained decrease in weight from P30 onward. Second, the high-dose SOD1 G93A mice reached end stage ϳ8 days (ϳ6% decrease in life span) sooner than vehicle and low-dose animals because of an increased rate of motor impairment. Fluoxetine increases synaptic serotonin (5-HT) levels, which is known to increase spinal motoneuron excitability. We confirmed that 5-HT increases spinal motoneuron excitability during this neonatal time period and therefore hypothesized that antagonizing 5-HT receptors during the same time period would improve disease outcome. However, cyproheptadine (1 or 5 mg/kg), a 5-HT receptor antagonist, had no effect on disease progression. These results show that a brief period of antidepressant treatment during a critical time window (the transition from neonatal to juvenile states) can be detrimental in ALS mouse models. amyotrophic lateral sclerosis; motoneuron excitability; fluoxetine; Prozac; antidepressant

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Amyotrophic lateral sclerosis: changes of noradrenergic and serotonergic transmitter systems in the spinal cord

Cited by 46 publications

References 43 publications

CSF markers in amyotrophic lateral sclerosis

CSF markers in amyotrophic lateral sclerosis

Potential links between neurological disease and Tako-Tsubo cardiomyopathy: A literature review

Effect of fluoxetine on disease progression in a mouse model of ALS

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