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Upregulation of Bax protein and increased DNA degradation in ALS spinal cord motor neurons
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Neuroscience.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurology.
1999 (English)In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 100, no 5, 317-321 p.Article in journal (Refereed) Published
Abstract [en]

Objectives

To investigate if degeneration of motor neurons in amyotrophic lateral sclerosis (ALS) is related to altered levels of the apoptosis regulating proteins Bcl-2 and Bax. In addition, immunoreactivity of the cysteine protease ICH-1L and detection of motor neurons with DNA fragmentation, indicative of apoptosis, was also studied.

Material and methods

The immunoreactivity of Bcl-2, Bax and ICH-1L were compared in ALS and control spinal cord motor neurons by immunohistochemical analysis and motor neurons with DNA fragmentation were identified by the TUNEL-method.

Results

The results demonstrate an increased expression of Bax in the ALS material as compared to controls but no change in Bcl-2 and ICH-1L expressions. Moreover, a larger proportion of motor neurons stained positive for TUNEL in ALS spinal cords.

Conclusion

Present study suggest an upregulation of the cell death promoting protein Bax and increased DNA degradation, indicative of apoptosis, in spinal motor neurons of ALS patients.

Place, publisher, year, edition, pages
1999. Vol. 100, no 5, 317-321 p.
Keyword [en]
amyotrophic lateral sclerosis (ALS), Bcl-2, bax, ICH-1L, neurodegeneration, TUNEL
National Category
Basic Medicine
Identifiers
URN: urn:nbn:se:uu:diva-55934ISI: 000083155400007PubMedID: 10536919OAI: oai:DiVA.org:uu-55934DiVA: diva2:83842
Available from: 2008-10-17 Created: 2008-10-17 Last updated: 2017-12-04Bibliographically approved

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