Manganese, Selenium and Other Trace Elements in Spinal Cord, Liver and Bone in Motor Neurone Disease

Mitchell, John D.; East, B.W.; Harris, IA; Pentland, Brian T.

doi:10.1159/000116626

Cited by 44 publications

(14 citation statements)

References 10 publications

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“…Some studies in other locations found increased Mn levels in brain, spinal cord, and muscle from ALS patients (Kurlander and Patten, 1979; Mitchell et al, 1991; Miyata et al, 1983) while others did not (Kihira et al, 1990; Pierce-Ruhland and Patten, 1980). Most of these studies were small, however, and the observed changes in Mn levels may reflect tissue degeneration.…”

Section: Discussionmentioning

confidence: 97%

Blood levels of trace metals and amyotrophic lateral sclerosis

et al. 2016

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Some trace metals may increase risk of amyotrophic lateral sclerosis (ALS), whereas others may be beneficial. Our goal was to examine associations of ALS with blood levels of selenium (Se), zinc (Zn), copper (Cu), and manganese (Mn). We conducted a case-control study of 163 neurologist confirmed patients from the National Registry of Veterans with ALS and 229 frequency-matched veteran controls. We measured metal levels in blood using inductively coupled plasma mass spectrometry and estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between ALS and a doubling of metal levels using unconditional logistic regression, adjusting for age, gender, and race/ethnicity. ALS was inversely associated with both Se (OR=0.4, 95% CI: 0.2–0.8) and Zn (OR=0.4, 95% CI: 0.2–0.8). Inverse associations with Se were stronger in patients with bulbar compared to spinal onset, worse function, longer diagnostic delay, and longer collection delay; inverse associations with Zn were stronger for those with worse function and longer collection delay. In contrast, ALS was positively associated with Cu (OR=3.4, 95% CI: 1.5–7.9). For Mn, no linear trend was evident (OR=0.9, 95% CI: 0.6–1.3, Ptrend=0.51). Associations of Se, Zn, Cu, and Mn with ALS were independent of one another. Adjustment for lead levels attenuated the positive association of ALS with Cu but did not change associations with Se, Zn, or Mn. In conclusion, Se and Zn were inversely associated with ALS, particularly among those with worse function, suggesting that supplementation with these metals may benefit such patients, while Cu was positively associated with ALS. Deficiencies of Se and Zn and excess Cu may have a role in ALS etiology.

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Section: Discussionmentioning

confidence: 97%

Blood levels of trace metals and amyotrophic lateral sclerosis

et al. 2016

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“…Mitchell et al [51] report a significant elevation of selenium within the cervical cords (as well as livers and bones) of motor neuron disease patients. However, a similar trend is absent in the thoracic and lumbar spines.…”

Section: Seleniummentioning

confidence: 99%

The Association of Exposure to Lead, Mercury, and Selenium and the Development of Amyotrophic Lateral Sclerosis and the Epigenetic Implications

et al. 2010

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Metal exposures are an intriguing potential culprit in the cause of sporadic amyotrophic lateral sclerosis (ALS). For one, there are numerous case reports linking different metals to an ALS phenotype. Furthermore, some investigators have demonstrated higher levels of certain metals in the blood, bone, cerebrospinal fluid, urine, or spinal cords of patients with ALS compared to controls. There are also many case-control studies looking at the possible association of certain metals with the development of ALS. We have reviewed the relevant literature regarding metal exposures and the risk of developing ALS. We found that many different metals have been implicated as having a role in ALS, but there is more literature investigating the role of lead than any other metal. Despite many studies, the role, if any, of this metal in the pathogenesis of ALS remains unclear. Similarly, other metals either have inconclusive, conflicting, or insufficient results in order to make a definitive conclusion. One explanation for these findings is that metal exposures alone are insufficient for the development of ALS. Perhaps an interaction between the metal exposure and an individual’s genetic makeup is required to produce epigenetic changes that ultimately lead to ALS.

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“…ALS arising in a patient affected by liver cirrhosis, a condition known to imply Mn overload due to impaired biliary excretion of the metal [174], has also been observed [175]. Mn overload has been reported in pathological and analytical studies of Guamanian and sporadic ALS cases [176, 177, 178, 179, 180]; the last two studies also showed an increase in MnSOD levels in motor neurons of affected subjects. Indeed, environmental data from the Western Pacific endemic foci of ALS, including the Kii peninsula in Japan, support a role for Mn in its prevalence in these areas [181, 182] and contribute to what is generally called “the mineral hypothesis” of the ALS/Parkinson’s Dementia Complex (ALS/PDC).…”

Section: Mn and Amyotrophic Lateral Sclerosis (Als)mentioning

confidence: 99%