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1 dults as a progressive spinal cord syndrome (adrenomyeloneuropathy).
2 metabolism, such as adrenoleukodystrophy and adrenomyeloneuropathy.
3 ave a poor prognosis owing to development of adrenomyeloneuropathy.
4 ted ABCD1 delivery to the brain in mice with adrenomyeloneuropathy.
5 gic pathway may contribute to dysfunction in adrenomyeloneuropathy.
6 le of neuronal ABCD1 in mice and humans with adrenomyeloneuropathy.
7 arkers of disease progression in adults with adrenomyeloneuropathy.
9 hy has two distinct neurological phenotypes: adrenomyeloneuropathy, a non-inflammatory axonopathy mos
10 had established severe motor disability from adrenomyeloneuropathy affecting only the spinal cord and
11 hich manifests as the spinal cord axonopathy adrenomyeloneuropathy (AMN) in nearly all males survivin
14 ly variable, ranging from slowly progressive adrenomyeloneuropathy (AMN) to life-threatening inflamma
15 ween ALD phenotypes in patients with cALD or adrenomyeloneuropathy (AMN), heterozygote female carrier
17 ing from progressive spinal cord axonopathy [adrenomyeloneuropathy (AMN)] to severe demyelination and
18 a cross-sectional study on 13 patients with adrenomyeloneuropathy and 12 age-matched healthy control
20 ionally, a large proportion of patients with adrenomyeloneuropathy develop life-threatening progressi
22 2), neoplasia (n = 2), genetically confirmed adrenomyeloneuropathy (n = 1), and other conditions (n =
23 , a life-threatening event for patients with adrenomyeloneuropathy, occurred only in patients in the
26 hological features in a mouse model of human Adrenomyeloneuropathy, preceding disease-onset by one ye
27 l changes that can characterize the brain of adrenomyeloneuropathy subjects in the early stages of th