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Trends Mol Med. 2016 Sep;22(9):769-783. doi: 10.1016/j.molmed.2016.07.005. Epub 2016 Aug 4.

Common Molecular Pathways in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.

Author information

1
Department of Neurology, Charcot Professorship, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany. Electronic address: jochen.weishaupt@uni-ulm.de.
2
Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstra├če 108, 01307 Dresden, Germany. Electronic address: hyman@mpi-cbg.de.
3
Institute of Biochemistry II, Goethe University School of Medicine, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany; Buchmann Institute for Molecular Life Sciences, Goethe University, Max-von-Laue-Strasse 15, 60438 Frankfurt am Main, Germany. Electronic address: ivan.dikic@biochem2.de.

Abstract

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are age-related neurodegenerative diseases in which predominantly motor neurons and cerebral cortex neurons, respectively, are affected. Several novel ALS and FTD disease genes have been recently discovered, pointing toward a few overarching pathways in ALS/FTD pathogenesis. Nevertheless, a precise picture of how various cellular processes cause neuronal death, or how different routes leading to ALS and FTD are functionally connected is just emerging. Moreover, how the most recent milestone findings in the ALS/FTD field might lead to improved diagnosis and treatment is actively being explored. We highlight some of the most exciting recent topics in the field, which could potentially facilitate the identification of further links between the pathogenic ALS/FTD pathways related to autophagy, vesicle trafficking, and RNA metabolism.

KEYWORDS:

RNA granules; amyotrophic lateral sclerosis; autophagy; frontotemporal dementia; genetics

PMID:
27498188
DOI:
10.1016/j.molmed.2016.07.005
[Indexed for MEDLINE]

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