Plasma proteome profiling identifies changes associated to AD but not to FTD

Table 1 Demographics

	n (%)	Age, years mean (SD)^a	Sex, female, n (%)	MMSE, mean (SD)	Post-mortem delay mean (SD) in hours
Plasma
FTD	56 (22%)	59.4 (7.4)	25 (45%)	24 (5.2)
FTLD-TDP^d	40 (71%)	59.8 (7.9)	18 (45%)	24 (5.7)
FTLD-Tau^e	16 (29%)	58.2 (6.2)	7 (44%)	25 (3.6)
AD	57 (22%)	65.5 (8.0)^c	22 (39%)	23 (2.3)
Controls	148 (57%)	61.3 (7.9)	60 (41%)	29 (1.4) ^b
Post-mortem frontal cortex
FTD	10 (67%)	60.1 (8.0)	6 (60%)	NA	6.5 (3.7)
FTLD-TDP	5 (50%)	64.0 (7.7)	3 (60%)	NA	6.8 (3.1)
FTLD-Tau	5 (50%)	56.2 (6.9)	3 (60%)	NA	5.3 (0.6)
Controls	4 (33%)	61.3 (8.1)	3 (75%)	NA	8.8 (2.5)

Analysis of variance (ANOVA) or Kruskal–Wallis test were used as appropriate. p < 0.05 was considered significant
AD Alzheimer’s disease, TDP TAR DNA binding protein 43, FTD frontotemporal lobar degeneration, MMSE mini mental state examination, NA not available
^aAge at inclusion in plasma samples and age at death in post-mortem tissue
^bFTD patients and AD had significantly lower MMSE scores
^cFTD patients and controls were significantly younger than AD patients
^dFTLD-TDP pathology was present in 40 subjects (18 autopsy confirmed cases, 13 GRN [of whom 1 was autopsy confirmed], 9 C9orf72 [of whom 1 was autopsy confirmed]), and FTLD-Tau pathology in 16 subjects (3 autopsy-confirmed cases, 13 MAPT [of whom 2 were also autopsy confirmed])
^eFTLD-TDP was present in 5 subjects (4 cases were familial [GRN n = 2 and C9orf72 n = 2] and 1 was a sporadic case), and FTLD-Tau was present in 5 cases (all 5 cases were familial [MAPT n = 5])

ISSN: 2051-5960