Regulation of melatonin and neurotransmission in Alzheimer’s disease

Jaydeep Roy; Ka Chun Tsui; Jonah Ng; Man Lung Fung; Lee Wei Lim

doi:10.3390/ijms22136841

Regulation of melatonin and neurotransmission in Alzheimer’s disease

Jaydeep Roy, Ka Chun Tsui, Jonah Ng, Man Lung Fung, Lee Wei Lim^*

^*Corresponding author for this work

The University of Hong Kong

Research output: Contribution to journal › Review article › peer-review

36 Citations (Scopus)

Abstract

Alzheimer’s disease is a neurodegenerative disorder associated with age, and is character-ized 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.

Original language	English
Article number	6841
Journal	International Journal of Molecular Sciences
Volume	22
Issue number	13
DOIs	https://doi.org/10.3390/ijms22136841
Publication status	Published - 1 Jul 2021
Externally published	Yes

Keywords

Alzheimer’s disease
Melatonin
Neurotransmission

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10.3390/ijms22136841

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title = "Regulation of melatonin and neurotransmission in Alzheimer{\textquoteright}s disease",

abstract = "Alzheimer{\textquoteright}s disease is a neurodegenerative disorder associated with age, and is character-ized 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.",

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AU - Roy, Jaydeep

AU - Tsui, Ka Chun

AU - Ng, Jonah

AU - Fung, Man Lung

AU - Lim, Lee Wei

PY - 2021/7/1

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N2 - Alzheimer’s disease is a neurodegenerative disorder associated with age, and is character-ized 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.

AB - Alzheimer’s disease is a neurodegenerative disorder associated with age, and is character-ized 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.

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Regulation of melatonin and neurotransmission in Alzheimer’s disease

Abstract

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