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. 2010 Jan 15;15(3):555–571. doi: 10.1111/j.1582-4934.2010.01011.x

Table 1.

Pathological, genetic, clinical data and expression of TGF-β1 in cerebral cortex, white matter and caudate nucleus of eight control subjects, six patients with original pathological diagnosis of HD and one asymptomatic subject

Patients Age in years Gender Vonsattel et al.’s Grade CAG repeats Brain weight (g) Clinical diagnosis of HD TGF-β1immunoreactivity*
Cerebral cortex White matter Caudate nucleus
1 59 F 0 - 1456 - 2 0 2
2 73 M 0 - 1389 - 2 0 1
3 66 F 0 - 1463 - 3 0 2
4 61 M 0 - 1510 - 3 0 1
5 68 F 0 - 1478 - 2 0 1
6 67 M 0 - 1470 - 2 0 1
7 59 F 0 - 1480 - 3 0 1
8 64 M 0 - 1420 - 2 0 2
Mean ± S.E.M. 64.6 ± 1.8 2.4 ± 0.2 1.4 ± 0.2
9 67 M III 9/43 1185 + 1 2 3
10 61 F III 22/44 1070 + 1 2 4
11 60 F III-IV 20/46 825 + 2 3 3
12 61 F III 25/44 800 + 1 3 3
13 59 M III 19/42 1330 + 2 2 4
14 67 M III-IV 20/45 1160 + 1 2 4
Mean ± S.E.M. 62.5 ± 1.6 1.3 ± 0.2 2.3 ± 0.2 3.5 ± 0.2
15 39 F 0 ND# ND At risk 0 1

Subjects 1–8= Healthy controls; subjects 9–14= Symptomatic HD patients, subjects 15= asymptomatic subjects (positive genetic test of HD and unreported CAG size #). HD: Huntington disease; (0)= negative; (1)= light; (2)= moderate; (3)= strong. *P <0.05 (Student’s t-test) HD versus non-HD patients.