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Publications

Journal Article Review Ppublish 6 citations

PubMed: 39012443 DOI: 10.1007/s12035-024-04333-y

An Expanded Narrative Review of Neurotransmitters on Alzheimer's Disease: The Role of Therapeutic Interventions on Neurotransmission.

Mol Neurobiol 62(2):1631-1674

Authors: Enes Akyuz, Alina Arulsamy, Feyza Sule Aslan, Bugra Sarisözen, Beyzanur Guney, Abdulhekim Hekimoglu, Beyza Nur Yilmaz, Thaarvena Retinasamy, Mohd Farooq Shaikh

Affiliations

  • Department of Biophysics, International School of Medicine, University of Health Sciences, Istanbul, Turkey.
  • Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
  • Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Selangor, Malaysia.
  • School of Medicine, Marmara University, Istanbul, Turkey.
  • School of Medicine, Tekirdağ Namık Kemal University, Tekirdağ, Turkey.
  • International School of Medicine, University of Health Sciences, Istanbul, Turkey.
  • Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Selangor, Malaysia.
  • Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Selangor, Malaysia.
  • School of Dentistry and Medical Sciences, Charles Sturt University, Orange, New South Wales, 2800, Australia.

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease. The accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles are the key players responsible for the pathogenesis of the disease. The accumulation of Aβ plaques and tau affect the balance in chemical neurotransmitters in the brain. Thus, the current review examined the role of neurotransmitters in the pathogenesis of Alzheimer's disease and discusses the alterations in the neurochemical activity and cross talk with their receptors and transporters. In the presence of Aβ plaques and neurofibrillary tangles, changes may occur in the expression of neuronal receptors which in turn triggers excessive release of glutamate into the synaptic cleft contributing to cell death and neuronal damage. The GABAergic system may also be affected by AD pathology in a similar way. In addition, decreased receptors in the cholinergic system and dysfunction in the dopamine neurotransmission of AD pathology may also contribute to the damage to cognitive function. Moreover, the presence of deficiencies in noradrenergic neurons within the locus coeruleus in AD suggests that noradrenergic stimulation could be useful in addressing its pathophysiology. The regulation of melatonin, known for its effectiveness in enhancing cognitive function and preventing Aβ accumulation, along with the involvement of the serotonergic system and histaminergic system in cognition and memory, becomes remarkable for promoting neurotransmission in AD. Additionally, nitric oxide and adenosine-based therapeutic approaches play a protective role in AD by preventing neuroinflammation. Overall, neurotransmitter-based therapeutic strategies emerge as pivotal for addressing neurotransmitter homeostasis and neurotransmission in the context of AD. This review discussed the potential for neurotransmitter-based drugs to be effective in slowing and correcting the neurodegenerative processes in AD by targeting the neurochemical imbalance in the brain. Therefore, neurotransmitter-based drugs could serve as a future therapeutic strategy to tackle AD.

MeSH

Neurofibrillary Tangles, Neurobiology, Alzheimer Disease, Pharmaceutical Preparations, Brain, Pathology, Therapeutics, Synaptic Transmission, Cognition

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