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Phosphorylated tau in plasma could be a biomarker of lower motor neuron impairment in amyotrophic lateral sclerosis.

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Title: Phosphorylated tau in plasma could be a biomarker of lower motor neuron impairment in amyotrophic lateral sclerosis.
Authors: Verde, Federico (AUTHOR), Milone, Ilaria (AUTHOR), Colombo, Eleonora (AUTHOR), Maranzano, Alessio (AUTHOR), Dubini, Antonella (AUTHOR), Colombrita, Claudia (AUTHOR), Gentile, Francesco (AUTHOR), Doretti, Alberto (AUTHOR), Torre, Silvia (AUTHOR), Messina, Stefano (AUTHOR), Morelli, Claudia (AUTHOR), Torresani, Erminio (AUTHOR), Poletti, Barbara (AUTHOR), Priori, Alberto (AUTHOR), Maderna, Luca (AUTHOR), Ratti, Antonia (AUTHOR), Silani, Vincenzo (AUTHOR), Ticozzi, Nicola (AUTHOR)
Source: Neurological Sciences. Oct2023, Vol. 44 Issue 10, p3697-3702. 6p. 2 Charts, 1 Graph.
Subjects: National Football League, Amyotrophic lateral sclerosis, Motor neurons, Tau proteins, Transcranial magnetic stimulation, Glomerular filtration rate
Abstract: Introduction: Plasma levels of phosphorylated tau (P-tau181) have been recently reported to be increased in amyotrophic lateral sclerosis (ALS) and associated with lower motor neuron (LMN) impairment. Patients and methods: We quantified plasma P-tau181 (pP-tau181) in a cohort of 29 deeply phenotyped ALS patients using the new fully automated Lumipulse assay and analysed phenotype-biomarker correlations. Results: pP-tau181 levels correlated positively with a clinical LMN score (r = 0.3803) and negatively, albeit not significantly, with a composite index of muscle strength (r = − 0.3416; p = 0.0811), but not with Penn Upper Motor Neuron (UMN) Score. Accordingly, pP-tau181 correlated with electromyographic indices of spinal active and chronic denervation (r = 0.4507 and r = 0.3864, respectively) but not with transcranial magnetic stimulation parameters of UMN dysfunction. pP-tau181 levels did not correlate with those in the cerebrospinal fluid (CSF), serum NFL, serum GFAP, CSF/serum albumin ratio, or estimated glomerular filtration rate, but correlated with plasma creatine kinase levels (r = 0.4661). Finally, while not being associated with neuropsychological phenotype, pP-tau181 correlated negatively with pH (r = − 0.5632) and positively with partial pressure of carbon dioxide (PaCO2; r = 0.7092), bicarbonate (sHCO3−; r = 0.6667) and base excess (r = 0.6611) on arterial blood gas analysis. Discussion: pP-tau181 has potential as ALS biomarker and could be associated with LMN impairment. Its raised levels might reflect pathophysiological processes (tau hyperphosphorylation and/or release) occurring in the axons of LMNs distantly from the CNS and the CSF. pP-tau181 could also be associated with respiratory dysfunction. [ABSTRACT FROM AUTHOR]
Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Phosphorylated tau in plasma could be a biomarker of lower motor neuron impairment in amyotrophic lateral sclerosis.
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  Data: <searchLink fieldCode="JN" term="%22Neurological+Sciences%22">Neurological Sciences</searchLink>. Oct2023, Vol. 44 Issue 10, p3697-3702. 6p. 2 Charts, 1 Graph.
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  Data: <searchLink fieldCode="DE" term="%22National+Football+League%22">National Football League</searchLink><br /><searchLink fieldCode="DE" term="%22Amyotrophic+lateral+sclerosis%22">Amyotrophic lateral sclerosis</searchLink><br /><searchLink fieldCode="DE" term="%22Motor+neurons%22">Motor neurons</searchLink><br /><searchLink fieldCode="DE" term="%22Tau+proteins%22">Tau proteins</searchLink><br /><searchLink fieldCode="DE" term="%22Transcranial+magnetic+stimulation%22">Transcranial magnetic stimulation</searchLink><br /><searchLink fieldCode="DE" term="%22Glomerular+filtration+rate%22">Glomerular filtration rate</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Introduction: Plasma levels of phosphorylated tau (P-tau181) have been recently reported to be increased in amyotrophic lateral sclerosis (ALS) and associated with lower motor neuron (LMN) impairment. Patients and methods: We quantified plasma P-tau181 (pP-tau181) in a cohort of 29 deeply phenotyped ALS patients using the new fully automated Lumipulse assay and analysed phenotype-biomarker correlations. Results: pP-tau181 levels correlated positively with a clinical LMN score (r = 0.3803) and negatively, albeit not significantly, with a composite index of muscle strength (r = − 0.3416; p = 0.0811), but not with Penn Upper Motor Neuron (UMN) Score. Accordingly, pP-tau181 correlated with electromyographic indices of spinal active and chronic denervation (r = 0.4507 and r = 0.3864, respectively) but not with transcranial magnetic stimulation parameters of UMN dysfunction. pP-tau181 levels did not correlate with those in the cerebrospinal fluid (CSF), serum NFL, serum GFAP, CSF/serum albumin ratio, or estimated glomerular filtration rate, but correlated with plasma creatine kinase levels (r = 0.4661). Finally, while not being associated with neuropsychological phenotype, pP-tau181 correlated negatively with pH (r = − 0.5632) and positively with partial pressure of carbon dioxide (PaCO2; r = 0.7092), bicarbonate (sHCO3−; r = 0.6667) and base excess (r = 0.6611) on arterial blood gas analysis. Discussion: pP-tau181 has potential as ALS biomarker and could be associated with LMN impairment. Its raised levels might reflect pathophysiological processes (tau hyperphosphorylation and/or release) occurring in the axons of LMNs distantly from the CNS and the CSF. pP-tau181 could also be associated with respiratory dysfunction. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: <i>Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1007/s10072-023-06916-4
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        Text: English
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