Regulation of Melatonin and Neurotransmission in Alzheimer's Disease

Int J Mol Sci. 2021 Jun 25;22(13):6841. doi: 10.3390/ijms22136841.

Abstract

Alzheimer's disease is a neurodegenerative disorder associated with age, and is characterized by pathological markers such as amyloid-beta plaques and neurofibrillary tangles. Symptoms of AD include cognitive impairments, anxiety and depression. It has also been shown that individuals with AD have impaired neurotransmission, which may result from the accumulation of amyloid plaques and neurofibrillary tangles. Preclinical studies showed that melatonin, a monoaminergic neurotransmitter released from the pineal gland, is able to ameliorate AD pathologies and restore cognitive impairments. Theoretically, inhibition of the pathological progression of AD by melatonin treatment should also restore the impaired neurotransmission. This review aims to explore the impact of AD on neurotransmission, and whether and how melatonin can enhance neurotransmission via improving AD pathology.

Keywords: Alzheimer’s disease; melatonin; neurotransmission.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / etiology
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism
  • Biogenic Monoamines / metabolism
  • Disease Susceptibility
  • Humans
  • Melatonin / metabolism*
  • Neurofibrillary Tangles / metabolism
  • Neurofibrillary Tangles / pathology
  • Neurotransmitter Agents / metabolism*
  • Phosphorylation
  • Plaque, Amyloid / metabolism
  • Plaque, Amyloid / pathology
  • Synaptic Transmission*
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • Biogenic Monoamines
  • Neurotransmitter Agents
  • tau Proteins
  • Melatonin