» Articles » PMID: 15372249

Rasagiline Alone and in Combination with Riluzole Prolongs Survival in an ALS Mouse Model

Overview
Journal J Neurol
Specialty Neurology
Date 2004 Sep 17
PMID 15372249
Citations 42
Authors
Affiliations
Soon will be listed here.
Abstract

Rasagiline is an antiapoptotic compound with neuroprotective potential. We examined its neuroprotective effect alone and in combination with the putative glutamate release blocker riluzole in the G93A model of familial amyotrophic lateral sclerosis (fALS). Endpoints of experimental treatment were survival and motor activity. The drug had a significant dose-dependent therapeutic effect on both preclinical and clinical motor function and survival of the animals. We also found that the combination of rasagiline with riluzole is safe and increases survival by about 20 % in a dose-dependent manner. Therefore, we conclude that the combination of rasagiline and riluzole is a promising clinical combination for the improvement of current neuroprotective treatment strategies of ALS.

Citing Articles

Discovery of Novel Inhibitors against ALS-Related SOD1(A4V) Aggregation through the Screening of a Chemical Library Using Differential Scanning Fluorimetry (DSF).

Giannakou M, Akrani I, Tsoka A, Myrianthopoulos V, Mikros E, Vorgias C Pharmaceuticals (Basel). 2024; 17(10).

PMID: 39458929 PMC: 11510448. DOI: 10.3390/ph17101286.


A new potential therapeutic approach for ALS: A case report with NGS analysis.

Hu C, Chen P, Padmanabhan N, Zahn A, Ho C, Wang K Medicine (Baltimore). 2024; 103(9):e37401.

PMID: 38428880 PMC: 10906646. DOI: 10.1097/MD.0000000000037401.


Mitochondria: A Promising Convergent Target for the Treatment of Amyotrophic Lateral Sclerosis.

Cunha-Oliveira T, Montezinho L, Simoes R, Carvalho M, Ferreiro E, Silva F Cells. 2024; 13(3.

PMID: 38334639 PMC: 10854804. DOI: 10.3390/cells13030248.


In-depth analysis of data from the RAS-ALS study reveals new insights in rasagiline treatment for amyotrophic lateral sclerosis.

Schuster J, Dreyhaupt J, Monkemoller K, Dupuis L, Dieterle S, Weishaupt J Eur J Neurol. 2024; 31(4):e16204.

PMID: 38240416 PMC: 11235627. DOI: 10.1111/ene.16204.


Pathophysiology of ion channels in amyotrophic lateral sclerosis.

Stringer R, Weiss N Mol Brain. 2023; 16(1):82.

PMID: 38102715 PMC: 10722804. DOI: 10.1186/s13041-023-01070-6.


References
1.
Turner M, Bakker M, Sham P, Shaw C, Leigh P, Al-Chalabi A . Prognostic modelling of therapeutic interventions in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord. 2002; 3(1):15-21. DOI: 10.1080/146608202317576499. View

2.
Wong P, Pardo C, Borchelt D, Lee M, Copeland N, Jenkins N . An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria. Neuron. 1995; 14(6):1105-16. DOI: 10.1016/0896-6273(95)90259-7. View

3.
Ferrante R, Shinobu L, Schulz J, Matthews R, Thomas C, Kowall N . Increased 3-nitrotyrosine and oxidative damage in mice with a human copper/zinc superoxide dismutase mutation. Ann Neurol. 1997; 42(3):326-34. DOI: 10.1002/ana.410420309. View

4.
Ludolph A, Meyer T, Riepe M . Antiglutamate therapy of ALS--which is the next step?. J Neural Transm Suppl. 1999; 55:79-95. DOI: 10.1007/978-3-7091-6369-6_8. View

5.
Cleveland D, Rothstein J . From Charcot to Lou Gehrig: deciphering selective motor neuron death in ALS. Nat Rev Neurosci. 2001; 2(11):806-19. DOI: 10.1038/35097565. View