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Manganese and the brain.

Karin Tuschl1, Philippa B Mills, Peter T Clayton

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International Review of Neurobiology
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PubMed
Summary
This summary is machine-generated.

Manganese (Mn) is vital for cell function but toxic at high levels. Research explores Mn transport, neurotoxicity mechanisms, and treatments like chelation therapy for disorders such as manganism.

Keywords:
IronManganeseManganismNeurotoxicityParkinsonismSLC30A10

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Toxicology

Background:

  • Manganese (Mn) is an essential trace element crucial for cellular function and metabolism.
  • Despite its essentiality, Mn homeostasis mechanisms are not fully understood, and excess Mn causes neurotoxicity.
  • Several proteins are implicated in Mn transport, with SLC30A10 recently identified as a key human transporter.

Purpose of the Study:

  • To elucidate the mechanisms of manganese homeostasis and its transport across cells.
  • To detail the pathways and consequences of manganese neurotoxicity.
  • To review current and potential therapeutic strategies for manganese toxicity disorders.

Main Methods:

  • Review of existing literature on manganese transport proteins and homeostasis.
  • Analysis of studies investigating manganese neurotoxicity mechanisms, including effects on neurotransmission and cellular functions.
  • Examination of clinical presentations and diagnostic findings of manganese toxicity, including imaging.

Main Results:

  • Manganese homeostasis is tightly regulated, involving multiple transport proteins, with SLC30A10 playing a significant role.
  • Manganese neurotoxicity results from impaired neurotransmission (dopaminergic, glutamatergic, GABAergic), mitochondrial dysfunction, oxidative stress, and neuroinflammation.
  • Mn accumulation in the basal ganglia leads to movement disorders resembling Parkinson's disease (manganism).

Conclusions:

  • Understanding Mn transport and homeostasis is critical for addressing Mn toxicity.
  • Manganese neurotoxicity presents with distinct clinical and radiological features, particularly affecting the basal ganglia.
  • Treatment strategies involve reducing Mn body burden through chelation and managing associated deficiencies, like iron, to mitigate toxicity.