Abstract
BackgroundThe occurrence of Parkinson's disease (PD) is known to be associated both with increased nigrostriatal iron content and with low serum cholesterol and PD, but there has been no study to determine a potential relationship between these two factors.MethodsHigh-resolution MRI (T1-, T2, and multiple echo T2*-weighted imaging) and fasting lipid levels were obtained from 40 patients with PD and 29 healthy controls. Iron content was estimated from mean R2* values (R2* = 1/T2*) calculated for each nigrostriatal structure including substantia nigra, caudate, putamen, and globus pallidus. This was correlated with serum cholesterol levels after controlling for age, gender, and statin use.ResultsIn patients with PD, higher serum cholesterol levels were associated with lower iron content in the substantia nigra (R = −0.43, p = 0.011 for total-cholesterol, R = −0.31, p = 0.080 for low-density lipoprotein) and globus pallidus (R = −0.38, p = 0.028 for total-cholesterol, R = −0.27, p = 0.127 for low-density lipoprotein), but only a trend toward significant association of higher total-cholesterol with lower iron content in the striatum (R = −0.34, p = 0.052 for caudate; R = −0.32, p = 0.061 for putamen). After adjusting for clinical measures, the cholesterol-iron relationships held or became even stronger in the substantia nigra and globus pallidus, but weaker in the caudate and putamen. There was no significant association between serum cholesterol levels and nigrostriatal iron content for controls.ConclusionsThe data show that higher serum total-cholesterol concentration is associated with lower iron content in substantia nigra and globus pallidus in Parkinson's disease patients. Further studies should investigate whether this is mechanistic or epiphenomenological relationship.
Highlights
The etiology is known in a small percentage of genetically-linked cases, Parkinson’s disease (PD) is largely idiopathic, and likely involves interaction of host susceptibility and environmental factors
It is known that genetic alterations of some proteins involved in the regulation of iron homeostasis can cause brain iron accumulation and neurodegenerative disorders in humans [13,14]
Subjects Forty PD subjects and 29 controls were recruited from patients, their spouses, and relatives presenting to a tertiary movement disorders clinic
Summary
The etiology is known in a small percentage of genetically-linked cases, Parkinson’s disease (PD) is largely idiopathic, and likely involves interaction of host susceptibility (determined by our genome and/or behavior) and environmental factors. It is known that genetic alterations of some proteins involved in the regulation of iron homeostasis can cause brain iron accumulation and neurodegenerative disorders in humans [13,14]. These disorders, grouped under the name ‘‘neurodegeneration with brain iron accumulation’’, [15] include pathothenate kinase-associated neurodegeneration (PKAN) [16], hereditary aceruloplasminemia [17], and neuroferritinopathy [18]. Iron regulatory protein-2 null mice that have alterations in brain iron homeostasis show neurodegeneration and develop movement abnormalities [19] These observations suggest the hypothesis that iron dysregulation may have an etiological role in neurodegenerative diseases. The occurrence of Parkinson’s disease (PD) is known to be associated both with increased nigrostriatal iron content and with low serum cholesterol and PD, but there has been no study to determine a potential relationship between these two factors
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