Min as pretreatment. Sections have been also examined microscopically for the look, severity and topographical distribution of immunostaining of A within brain parenchyma (as amyloid plaques) and cerebral NPPB Protein E. coli vessels (as CAA). A five-pointDavidson et al. Acta Neuropathologica Communications (2018) six:Web page 3 ofTable 1 Chosen demographic, genetic and Grancalcin/GCA Protein E. coli neuropathological specifics for 56 men and women with Down syndromeCase ID# 1 two three four 5 six 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 UKBBN ID# na na na na na na na BBN_2966 na na na na BBN_2963 na na BBN_17186 BBN_17189 BBN_17178 BBN_2981 na na BBN_2968 BBN_3356 BBN_16954 BBN_3365 na BBN_3438 BBN_16273 BBN_2978 na BBN_3020 BBN_3355 BBN_3358 BBN_3437 BBN_3353 BBN_3363 BBN_2990 BBN_3364 na na BBN_16835 BBN_3352 BBN_3439 BBN_2964 gender M F M M F M F M M F M M F F M F M F M F M M F M M M F F M M F M F F M M M M F M M F F F age 0.01 0.1 1.six 1.six 3 11 13 13 23 27 35 36 37 39 42 47 47 49 50 50 51 53 53 54 55 55 56 56 57 57 58 58 58 58 59 59 60 60 60 60 60 61 61 62 karyotype na na na na na na na 47XY21 na na na na 47XX21 na na na na na 47XY21 na na 47XY21 na na na na na na 47XY21 na 47XX21 na na na na na 47XY21 na na na na na na 47XX21 APOE na na na na na na na three,three na na na na three,4 na na na na three,four three,four na na 3,3 3,four 2,four 3,four na 3,three three,four three,three na 3,3 3,4 3,three two,three 2,3 3,three three,3 3,3 na na 3,three two,three 3,4 3,3 Thal 0 0 0 0 0 0 0 1 0 1 2 five five two 5 five five four 3 0 5 five 5 five five 5 5 five 5 5 five 5 5 5 5 five five 5 five five 5 five 5 five Braak 0 0 0 0 0 0 0 0 0 0 0 II I b* V VI III III II b* VI III VI VI VI V VI VI V VI V VI VI V VI VI VI VI 0 VI III VI VI V Allen CAA 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 three 1 1 1 0 1 1 2 3 2 1 1 1 three 1 1 3 2 1 three 2 two two 0 two two three 2 three Thal CAA 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 two 1 1 1 0 1 1 1 two 1 1 1 1 two 1 1 two 1 1 2 1 1 1 0 1 1 two 1Davidson et al. Acta Neuropathologica Communications (2018) 6:Page four ofTable 1 Chosen demographic, genetic and neuropathological specifics for 56 individuals with Down syndrome (Continued)Case ID# 45 46 47 48 49 50 51 52 53 54 55 56 UKBBN ID# BBN_2965 BBN_2967 BBN_3354 BBN_3441 na BBN_2969 BBN_3440 BBN_2975 BBN_17004 na na BBN_2985 gender M F M M M M F M M M F M age 62 62 62 62 63 64 64 65 65 66 69 76 karyotype 47XY21 47XX21 na na na 47XY21 na 47XY21 na na na 47XY21 APOE 3,3 3,3 3,three 2,three na three,three 3,3 3,3 three,three na na two,three Thal 5 5 five 5 5 five five 5 5 5 five 5 Braak V IV VI VI VI IV VI V V V VI III Allen CAA 1 three three 3 1 1 2 1 1 1 1 3 Thal CAA 1 2 2 two 1 1 1 1 1 1 1Thal = Thal phase of amyloid deposition and Braak = Braak tau stage. CAA phenotype was assessed in accordance with Allen et al. (2014) and Thal et al. (2010). UKBBN = UK Brain Bank Network ID number, na = not available/applicablescoring method [31, 37] was employed to separately grade the severity of plaques and CAA.PlaquesGrade 0 – no amyloid plaques in present. Grade 1 – A couple of amyloid plaques in each and every low energy (ten microscope objective) field. Grade 2 – A moderate quantity of amyloid plaques in each and every low energy field. Grade three – Numerous dispersed amyloid plaques in every low energy field. Grade four – Pretty numerous, densely packed amyloid plaques in each low energy field.CAAGrade 0 – No CAA in blood vessel walls in leptomeninges or brain parenchyma. Grade 1 – Occasional blood vessels with CAA in leptomeninges and/or brain parenchyma, commonly not occupying the full thickness with the wall. Grade two – A moderate number of blood vessels with CAA in leptomeninges and/or brain parenchyma, some occupying the complete thickness in the wall. Gr.