Mitochondrial Interaction with Serotonin in Neurobiology and Its Implication in Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is a lethal neurodegenerative disorder characterized by severe brain pathologies and progressive cognitive decline. While the exact cause of this disease remains unknown, emerging evidence suggests that dysregulation of neurotransmitters contributes to the development of AD pathology and symptoms. Serotonin, a critical neurotransmitter in the brain, plays a pivotal role in regulating various brain processes and is implicated in neurological and psychiatric disorders, including AD. Recent studies have shed light on the interplay between mitochondrial function and serotonin regulation in brain physiology. In AD, there is a deficiency of serotonin, along with impairments in mitochondrial function, particularly in serotoninergic neurons. Additionally, altered activity of mitochondrial enzymes, such as monoamine oxidase, may contribute to serotonin dysregulation in AD. Understanding the intricate relationship between mitochondria and serotonin provides valuable insights into the underlying mechanisms of AD and identifies potential therapeutic targets to restore serotonin homeostasis and alleviate AD symptoms. This review summarizes the recent advancements in unraveling the connection between brain mitochondria and serotonin, emphasizing their significance in AD pathogenesis and underscoring the importance of further research in this area. Elucidating the role of mitochondria in serotonin dysfunction will promote the development of therapeutic strategies for the treatment and prevention of this neurodegenerative disorder.

The 40 Hz flickering light restores synaptic plasticity and mitochondrial phenotype in experimental model of Alzheimer’s disease

“…In the dark, levels of dopamine are reduced in our body and are elevated during our light cycle of the day, as opposed to melatonin levels [16, 69, 70]. The increase we observed in the levels of both neurotransmitters might be due to elevated energy supply for synaptic activities, increased intracellular calcium levels, and light-induced neuronal activity [71, 72].…”