Dietary Melatonin Therapy Alleviates the Lamina Cribrosa Damages in Patients with Mild Cognitive Impairments: A

Lei Xu1, Haixiang Yu1, Hongbin Sun1

  • 1Department of Thoracic Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China (mainland).

Insights

Melatonin treatment may improve lamina cribrosa thickness (LCT) and hippocampus volume in patients with mild cognitive impairment (MCI). This dietary therapy could be an effective treatment for MCI, potentially aiding early diagnosis through LCT assessment.

Area of Science:

  • Neuroscience
  • Ophthalmology
  • Gerontology

Background:

  • Alzheimer's disease (AD) involves neuron loss in the hippocampus and cortex.
  • Mild cognitive impairment (MCI) represents a transitional phase between normal cognition and AD dementia.
  • Lamina cribrosa thickness (LCT) is a potential biomarker for neurodegenerative changes.

Purpose of the Study:

  • To investigate the effects of melatonin on lamina cribrosa thickness (LCT) in patients with mild cognitive impairment (MCI).
  • To explore the relationship between LCT, cognitive function, and neuroimaging markers in MCI.
  • To evaluate melatonin as a therapeutic intervention for MCI.

Main Methods:

  • Comparison of LCT between MCI patients and healthy controls.
  • Randomized controlled trial assigning MCI patients to melatonin treatment or placebo.
  • Assessment of LCT, hippocampus volume, and cerebrospinal fluid (CSF) T-tau levels.

Main Results:

  • MCI patients exhibited significantly reduced LCT compared to controls.
  • Lower Mini Mental State Examination (MMSE) scores, smaller hippocampus volumes, and elevated CSF T-tau levels correlated with thinner LCT.
  • Melatonin treatment significantly increased LCT and hippocampus volume, while decreasing CSF T-tau levels compared to placebo.

Conclusions:

  • LCT measurement may aid in the early diagnosis of MCI.
  • Dietary melatonin therapy shows promise as an effective treatment for MCI patients with LCT alterations.
  • Melatonin influences neurostructural and neurochemical markers associated with MCI progression.

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