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New transgenic ALS / FTD models on the rat‐walk
Author(s) -
Stegmüller Judith,
Synofzik Matthis
Publication year - 2016
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.13775
Subject(s) - frontotemporal dementia , amyotrophic lateral sclerosis , neuroscience , neurodegeneration , hippocampus , neurochemistry , genetically modified mouse , dementia , transgene , psychology , biology , neurology , medicine , gene , disease , genetics , pathology
This Editorial highlights a study by Huang and colleagues in the current issue of Journal of Neurochemistry. The authors introduce a novel ALS‐FTD (amyotrophic lateral sclerosis‐frontotemporal dementia) rat model to explore the role of the UBLQN2 gene that has previously been associated with familial ALS‐FTD. Over‐expression of ubiquilin 2 in the cortex (CTX) and hippocampus of the rat results in ubiquilin 2 aggregates and neurodegeneration together with cognitive deficits. The new rat model not only gives insight into potential molecular underpinnings of ALS‐FTD, but also represents an important new tool for future research and therapeutic approaches. Read the highlighted article ‘Increased Ubqln2 expression causes neuron death in transgenic rats’ on page 285 .