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Modulation of serine/threonine phosphatases by melatonin: therapeutic approaches in neurodegenerative diseases

Raquel L Arribas1, Alejandro Romero2, Javier Egea1,3,4

  • 1Instituto-Fundación Teófilo Hernando, Departamento de Farmacología y Terapéutica, Universidad Autónoma de Madrid, Madrid, Spain.

British Journal of Pharmacology
|May 22, 2018
PubMed

Insights

Melatonin decline with aging contributes to neurodegeneration. This review explores how melatonin may protect against neurodegenerative diseases by influencing phosphoprotein phosphatases and correcting altered phosphorylation rates.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Biochemistry

Background:

  • Melatonin is an endogenous hormone with declining levels during aging.
  • Aging-related melatonin reduction is linked to neurodegenerative disorders.
  • Neurodegenerative diseases involve shared toxic mechanisms including proteinopathy and oxidative stress.

Purpose of the Study:

  • To investigate melatonin's potential to rectify altered phosphorylation/dephosphorylation rates in neurodegenerative diseases.
  • To analyze if melatonin directly interacts with and protects phosphoprotein phosphatases.

Main Methods:

  • Literature review focusing on melatonin's role in neuroprotection.
  • Analysis of studies investigating melatonin's influence on phosphoprotein phosphatase activity.
  • Examination of direct interaction mechanisms between melatonin and these enzymes.

Main Results:

  • Melatonin's decline is associated with neurodegenerative conditions.
  • Melatonin shows potential in counteracting neurodegenerative pathways.
  • Evidence suggests melatonin may influence phosphoprotein phosphatase activity.

Conclusions:

  • Melatonin may offer neuroprotection by modulating phosphorylation/dephosphorylation balance.
  • Direct interaction of melatonin with phosphoprotein phosphatases is a potential therapeutic mechanism.
  • Further research is warranted to explore melatonin's therapeutic applications in neurodegenerative diseases.

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