Inflammation in the brain is a key sign of neurodegenerative diseases including ALS and FTD. But whether this immune response contributes or is a consequence of these diseases remains hotly debated.
Now, a research team led by University of California-San Francisco’s Leo Sugrue reports that inflammation may increase the susceptibility of developing FTD (Broce et al., 2018; see also Ferrari et al., 2014). The findings build on previous studies, led by University of California-San Francisco’s Zachary Miller, which found that people with FTD with TDP-43 pathology were more likely to have an autoimmune disease (Miller et al., 2016; Miller et al., 2013).
The findings appeared on January 9 in PLOS Medicine.
The researchers found, based on a genome-wide association analysis, significant genetic overlap between FTD and immune-related diseases including rheumatoid arthritis and ulcerative colitis. What’s more, these shared disease-linked SNPs cluster in genes important in the function of microglia -the same immune cells that may mediate the neuroinflammation increasingly implicated in the pathogenesis of C9orf72 ALS and FTD (Umoh et al., 2017; O’Rourke et al., 2016; for review, see Lall and Baloh, 2017).
The approach, known as “pleiotropy” analysis, suggests that these diseases may share common immune-mediated mechanisms.
The results come at the heels of previous preclinical studies, led by University College London’s Adrian Isaacs in England, which found that the activation of microglia could be detected prior to neuronal loss in a mouse model of CHMP2B-linked FTD (see February 2017 news; Clayton et al., 2017).
Together, the findings add to growing evidence that inflammation may contribute to the onset of at least some forms of FTD. Therefore, emerging treatment strategies that reduce this inflammation may be a potential strategy to tackle them.
To learn more about the emerging role of inflammation in the onset of neurodegenerative diseases including ALS, check out Early Inflammation May Play A Role in FTD.
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