Regulation of Melatonin and Neurotransmission in Alzheimer’s Disease

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.

Analyzing the Effect of Weak External Transcranial Magnetic Stimulation on the Primary Dominant Frequencies of Alzheimer Patients Brain by Using MEG Recordings

“…However, the encouraging outcome with the up to now AD knowledge cannot be totally explicated. Still, one rational explanation might be the fact that weak magnetic fields hold a strong positive impact on the pineal gland's ability, through melatonin, to control endogenous opioid signal pathways [26][27][28] and several neurotransmission nets [29,30], which show significant changes in cognitive disorders. Additionally, another perspective is that this type of magnetic stimulation is capable of modulating neurons cell membrane's overall biological profile and role in the neurotransmission process, which is significantly impaired in AD patients [31].…”

Therapeutic Potential of Human Stem Cell Implantation in Alzheimer’s Disease

“…The N-methyl-D-aspartic acid (NMDA) receptor inhibitor and acetylcholinesterase inhibitor (AChEI) are two classes of approved medications for clinical use [ 62 ]. Acetylcholinesterase inhibitors (AChEls) act by inhibiting synaptic cleft cholinesterase from breaking down acetylcholine, thereby increasing cholinergic transmission in the cerebral cortex and basal forebrain [ 63 , 64 ]. Donepezil, rivastigmine, and galantamine are some examples of AChEI [ 65 ].…”

Synthesis, In Silico, and Biological Evaluation of a Borinic Tryptophan-Derivative That Induces Melatonin-like Amelioration of Cognitive Deficit in Male Rat

“…Moreover, melatonin administration improves the behavioral impairments related to AD in murine models, including disrupted circadian rhythm, cognition, learning, memory, motor function, mood, sleep, and stress response [ 6 , 7 ]. Furthermore, melatonin induces beneficial effects on the cholinergic system by increasing acetylcholine release and inhibiting choline acetyltransferase [ 7 ].…”

“…Moreover, melatonin administration improves the behavioral impairments related to AD in murine models, including disrupted circadian rhythm, cognition, learning, memory, motor function, mood, sleep, and stress response [ 6 , 7 ]. Furthermore, melatonin induces beneficial effects on the cholinergic system by increasing acetylcholine release and inhibiting choline acetyltransferase [ 7 ]. Furthermore, it also appears to exert benefits linked to the modulation of other monoamine systems, such as the serotonergic and dopaminergic systems by means of unestablished mechanisms [ 7 , 8 ].…”