## 2 Materials and Methods
### Participants  
Experimental data concern three AT patients with different ranges of severity of AT--they are described hereafter (the age of the patients is intended to be at the moment of experiment)--and three healthy subjects (male, 27 years old, 1.77 m, 75.4 kg; female, 22 years old, 1.66 m, 75 kg; male, 23 years old, 1.71 m, 76 kg), all of them walking at their comfortable speed (1.32, 0.2, 1.15, 1.13, 1.167, 1.2 m/s, respectively (the neurologically severe impairments of patient F are the cause of of the low walking speed)). The healthy subjects, who play the role of a (non-age matched) control group, are here used to assess the low magnitude of their \(\Phi\)-bonacci gait number, in light of the results of [25]. In particular, healthy subjects are selected as male/female controls in the age range 20-30 years and without any neurological or orthopedic deficits as representative of the physiology and biomechanics of mature walking. The features of the AT patients are reported hereafter. * [PERSON] is a 29-year-old woman who developed, by the age of 3 years, all the classic manifestations of AT; increased alpha-fetoprotein levels were initially detected. The diagnosis was confirmed by molecular analysis of the _ATM_ gene and the absence of ATM protein expression. Contrary to what was expected in the classic form of AT, by the age of 12 years, ataxia slowly disappeared, and a mild choreic movement disturbance has been the only neurologic finding since then. Now, she is an independent person who has obtained a satisfying job and practices sports. Her quality of life is said to be rather good by herself. A diagnosis of the mild form of AT was made at follow up. * [PERSON] is a 35-year-old man who began to show motor developmental troubles from 9 months of life, at which age he was hypotonic and lost the ability to keep a sitting position whereas wide based ambulation was evident at 23 months. Concurrently, intentional tremors, incoordination, and stance unsteadiness manifest. A diagnosis of AT was carried out when he was 3-years-old, on the grounds of his clinical examination, serum IgA deficiency, elevated alpha-fetoprotein, and atrophic cerebellar vermis. Molecular confirmation of _ATM_ gene mutations was obtained a few years later. Since the age of 11 yrs, [PERSON] has been able to stand and walk only with support, language has been dysarthric, and there have occurred truncal and gait ataxia, dystonic posture of neck and hands, marked choreo-atthethotic movements, and absent knees reflexes. The course of the disease was steadily progressive. At the present age of 37 yrs, he is neurologically severely impaired, can walk less than 10 m only with strong support, and is unable to sit for more than 10 min without continuous support. He pronounces only single words understandably. Since childhood, he has undergone respiratory physiotherapy at most twice a week, and, overall, for not more than 45 min per session. However, due to family job problems and the distance of his home from the hospital services, rehabilitative treatment has been, since the beginning, very discontinuous. [PERSON] has been diagnosed as being a long-term survivor patient with classic AT. * [PERSON] is a 7-year-old boy, the second born of apparently healthy parents. Early psychomotor milestones were normal until the age of 15 months, when a wide-based gait, unsteadiness, and dystonic posture of hands were noticed. At that time, a brain MRI was normal. However, due to the clinical picture, the elevated alpha-fetoprotein level, and the occurrence of the compound heterozygosity of the _ATM_ gene, a final diagnosis of AT was given. When examined at 2 yrs of age, clear truncal and gait ataxia, together with hand dystonia, were observed. Over the following 5 years, ataxia moderately worsened, and generalized hypotonia, muscle weakness with fine motor deficits and uncoordinated movements, marked drooling and brisk knee reflexes developed.