TY - JOUR
T1 - Neuroinflammation in frontotemporal dementia
AU - Bright, Fiona
AU - Werry, Eryn L.
AU - Dobson-Stone, Carol
AU - Piguet, Olivier
AU - Ittner, Lars M.
AU - Halliday, Glenda M.
AU - Hodges, John R.
AU - Kiernan, Matthew C.
AU - Loy, Clement T.
AU - Kassiou, Michael
AU - Kril, Jillian J.
PY - 2019/9/1
Y1 - 2019/9/1
N2 - Frontotemporal dementia (FTD) refers to a group of progressive neurodegenerative disorders with different pathological signatures, genetic variability and complex disease mechanisms, for which no effective treatments exist. Despite advances in understanding the underlying pathology of FTD, sensitive and specific fluid biomarkers for this disease are lacking. As in other types of dementia, mounting evidence suggests that neuroinflammation is involved in the progression of FTD, including cortical inflammation, microglial activation, astrogliosis and differential expression of inflammation-related proteins in the periphery. Furthermore, an overlap between FTD and autoimmune disease has been identified. The most substantial evidence, however, comes from genetic studies, and several FTD-related genes are also implicated in neuroinflammation. This Review discusses specific evidence of neuroinflammatory mechanisms in FTD and describes how advances in our understanding of these mechanisms, in FTD as well as in other neurodegenerative diseases, might facilitate the development and implementation of diagnostic tools and disease-modifying treatments for FTD.
AB - Frontotemporal dementia (FTD) refers to a group of progressive neurodegenerative disorders with different pathological signatures, genetic variability and complex disease mechanisms, for which no effective treatments exist. Despite advances in understanding the underlying pathology of FTD, sensitive and specific fluid biomarkers for this disease are lacking. As in other types of dementia, mounting evidence suggests that neuroinflammation is involved in the progression of FTD, including cortical inflammation, microglial activation, astrogliosis and differential expression of inflammation-related proteins in the periphery. Furthermore, an overlap between FTD and autoimmune disease has been identified. The most substantial evidence, however, comes from genetic studies, and several FTD-related genes are also implicated in neuroinflammation. This Review discusses specific evidence of neuroinflammatory mechanisms in FTD and describes how advances in our understanding of these mechanisms, in FTD as well as in other neurodegenerative diseases, might facilitate the development and implementation of diagnostic tools and disease-modifying treatments for FTD.
UR - http://www.scopus.com/inward/record.url?scp=85069489243&partnerID=8YFLogxK
UR - http://purl.org/au-research/grants/nhmrc/1132524
UR - http://purl.org/au-research/grants/nhmrc/1095127
UR - http://purl.org/au-research/grants/nhmrc/1140708
UR - http://purl.org/au-research/grants/nhmrc/1081916
UR - http://purl.org/au-research/grants/nhmrc/1138223
UR - http://purl.org/au-research/grants/nhmrc/1079679
UR - http://purl.org/au-research/grants/nhmrc/1136241
UR - http://purl.org/au-research/grants/nhmrc/1103258
UR - http://purl.org/au-research/grants/nhmrc/1107657
U2 - 10.1038/s41582-019-0231-z
DO - 10.1038/s41582-019-0231-z
M3 - Review article
C2 - 31324897
AN - SCOPUS:85069489243
VL - 15
SP - 540
EP - 555
JO - Nature Reviews Neurology
JF - Nature Reviews Neurology
SN - 1759-4758
IS - 9
ER -