A possible effect of montelukast on neurological aging examined by the use of register data
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RESEARCH ARTICLE
A possible effect of montelukast on neurological aging examined by the use of register data Bjørn Grinde1 · Henrik Schirmer2,3 · Anne Elise Eggen4 · Ludwig Aigner5 · Bo Engdahl1 Received: 23 April 2020 / Accepted: 17 September 2020 © The Author(s) 2020
Abstract Background The leukotriene receptor antagonist montelukast has been shown to rejuvenate aged brains in rats; however, data on humans are still scarce. Objective To investigate if montelukast may alleviate degenerative neurological changes using a register data. Setting Norwegian registry data analyses. Method The present observational study was based on data from the Norwegian Prescription Database and the Tromsø Study. The former has information regarding the use of prescription medicine; the latter includes tests for brain function such as subjective memory and finger-tapping. Multivariate linear regression analyses were performed to see how the use of various medications correlated with the test results, correcting for likely confounders. Main outcome measure Results on seven different tests considered relevant for neurological health were used as outcome. Results Previous use of montelukast correlated with improved scores on cognitive or neurological functioning (F = 2.20, p = 0.03 in a multivariate test). A range of other medications were tested with the same algorithm, including drugs acting on the immune system, but none of them correlated with (overall) significantly improved test results. Conclusion The present data suggest that montelukast may alleviate degenerative neurological changes associated with human aging. Keywords Anti-inflammatory medication · Dementia · Leukotriene · Montelukast · Neurological decline · Prescription database
Impacts on practice • The data suggest that montelukast may postpone mental
Introduction
sible effects on the brain.
The term ‘inflammaging’ has been coined for an elevated level of low-grade and sterile inflammation [1], which has been associated with age-related decline [2]. That is, inflammatory processes may be causally involved in the aging process in general, and in chronic neurodegenerative diseases such as dementias in particular [3–6]. In the case of dementias, inflammation could be one of the early pathological triggers [7]. Consequently, anti-inflammatory interventions have been proposed for treatment and/or prevention of agerelated diseases [8]. Targets for potential anti-inflammatory drugs are, among others, the pathways of the classical lipid-mediators of inflammation. These are for one, the arachidonic acidderived prostaglandins, a prominent pathway targeted by Cox1/2 inhibitors; and two, the leukotrienes, targeted by
* Bjørn Grinde [email protected]
Division of Mental and Physical Health, Norwegian Institute of Public Health, Oslo, Norway
2
Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway
3
Department of Cardiology, University Hospital North Norway, Tromsø, Norway
4
Department of Community Medicine, UiT The Arctic University of Norwa
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