期刊
JOURNAL OF MOLECULAR NEUROSCIENCE
卷 45, 期 3, 页码 516-521出版社
HUMANA PRESS INC
DOI: 10.1007/s12031-011-9555-x
关键词
Frontotemporal lobar degeneration; FTLD; FTLD-TDP; TMEM106B; Genome-wide association study; Genetic risk factor
资金
- Belgian Federal Science Policy office [P6/43]
- Foundation for Alzheimer Research (SAO/FRMA)
- Association for Frontotemporal Dementias (AFTD)
- Medical Foundation Queen Elisabeth
- Flemish Government
- Research Foundation Flanders (FWO)
- Institute for the Promotion of Innovation through Science and Technology in Flanders (IWT-V)
- University of Antwerp, Belgium
Recently, the first genome-wide association (GWA) study in frontotemporal lobar degeneration (FTLD) identified common genetic variability at the TMEM106B gene on chromosome 7p21.3 as a potential important risk-modifying factor for FTLD with pathologic inclusions of TAR DNA-binding protein (FTLD-TDP), the most common pathological subtype in FTLD. To gather additional evidence for the implication of TMEM106B in FTLD risk, multiple replication studies in geographically distinct populations were set up. In this review, we revise all recent replication and follow-up studies of the FTLD-TDP GWA study and summarize the growing body of evidence that establish TMEM106B as a bona fide risk factor for FTLD. With the TMEM106B gene, a new player has been identified in the pathogenic cascade of FTLD which could hold important implications for the future development of disease-modifying therapies.
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