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Functional Neuroimaging Using Ultrasonic Blood-brain Barrier Disruption and Manganese-enhanced MRI
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Published on: July 12, 2012

Role of manganese in neurodegenerative diseases

Aaron B Bowman1, Gunnar F Kwakye, Elena Herrero Hernández

  • 1Department of Neurology, Vanderbilt Kennedy Center, Center for Molecular Toxicology, Vanderbilt University Medical Center, Nashville, TN 37232-8552, United States.

Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS)
|October 4, 2011
PubMed

Insights

Manganese (Mn) is vital for health, but excess levels cause Parkinsonism. This review explores Mn transporters, its role in neurodegenerative diseases like Parkinson

Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Background:

  • Manganese (Mn) is an essential trace element crucial for development and homeostasis.
  • High Mn exposure can induce extrapyramidal symptoms similar to Parkinson's disease (PD).
  • Altered Mn homeostasis is implicated in various neurodegenerative disorders.

Purpose of the Study:

  • To review the role of transporters in brain Mn homeostasis.
  • To discuss Mn's involvement in idiopathic Parkinson's disease (IPD) and manganism.
  • To explore Mn's link to Huntington's disease (HD), Alzheimer's disease (AD), ALS, and prion disease.

Main Methods:

  • Literature review focusing on Mn homeostasis, neurodegenerative diseases, and Mn transport.
  • Discussion of similarities and differences between manganism and IPD.
  • Examination of Mn's role in protein aggregation and mitochondrial dysfunction.

Main Results:

  • Transporters play a key role in maintaining brain Mn levels.
  • Mn exposure shares mechanistic pathways with IPD, including alpha-synuclein aggregation and mitochondrial dysfunction.
  • Altered Mn homeostasis may contribute to HD pathogenesis.

Conclusions:

  • Mn homeostasis is critical for preventing neurotoxicity.
  • Mn's role in neurodegenerative diseases highlights potential therapeutic targets.
  • Further research into Mn's mechanisms in AD, ALS, and prion diseases is warranted.

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