Highlights
- •Factors affecting CSF lactate levels in neurodegenerative were investigated.
- •CSF lactate levels and CSF glucose levels showed a moderate positive correlation.
- •Age and CSF glucose levels influenced CSF lactate levels even after adjustment by multiple regression analysis.
- •Age and CSF glucose levels should be taken into consideration upon the use of CSF lactate levels as a biomarker.
Abstract
Despite recent studies examining the association between neurodegenerative diseases
and mitochondrial dysfunction, there are not sufficient data on factors that influence
cerebrospinal fluid (CSF) lactate levels. Thus, we investigated factors that affect
CSF lactate levels in neurodegenerative diseases. We extracted laboratory findings,
including CSF lactate, glucose, and protein levels, and demographic and background
information, including age and gender, from the electronic medical records of patients
with neurodegenerative diseases in order to explore factors that have an impact CSF
lactate levels. These patients had been admitted to our department and underwent a
CSF examination between April 2007 and March 2015. Data from 83 patients (average
age 64.5 years; 45 males and 38 females) were analyzed. The patients' diagnoses included amyotrophic
lateral sclerosis, multiple system atrophy, spinocerebellar degeneration, corticobasal
syndrome, Parkinson's disease, and Huntington's disease. CSF lactate levels were higher
in patients with a neurodegenerative disease who were aged 65 years and older relative to those who were aged under 65 years (p < 0.05), and CSF lactate and glucose levels showed a moderate positive correlation (r = 0.487). Age and CSF glucose levels influenced CSF lactate levels even after adjusting
for gender, age, CSF protein levels, and CSF glucose levels. When investigating CSF
lactate levels in neurodegenerative diseases, it is necessary to consider patients'
age and CSF glucose levels.
Keywords
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Article info
Publication history
Published online: April 20, 2017
Accepted:
April 19,
2017
Received in revised form:
March 27,
2017
Received:
November 30,
2016
Identification
Copyright
© 2017 Elsevier B.V. All rights reserved.
