ORCiD
Adam M. Kaye: 0000-0002-7224-3322
Document Type
Article
Publication Title
Neurology international
ISSN
2035-8385
Volume
14
Issue
2
DOI
10.3390/neurolint14020025
First Page
310
Last Page
321
Publication Date
3-22-2022
Abstract
Depression is a leading cause of disability globally, with a prevalence of 3.8% among the whole population, 5% of the adult population, and 5.7% of the elderly population over 60 years of age. There is evidence that depression is linked to certain neurodegenerative diseases, one being Alzheimer's disease (AD). The efficacy of conventional antidepressants to treat depression in AD is conflicting, especially regarding selective serotonin reuptake inhibitors (SSRIs). A recent systemic review and meta-analysis of 25 randomized controlled trials including fourteen antidepressant medications showed no high efficacy in treating AD patients' symptoms. However, ketamine, a nonselective N-methyl-D-aspartate (NMDA) receptor antagonist, can mediate a wide range of pharmacological effects, including neuroprotection, anti-inflammatory and anticancer properties, multimodal analgesia, and treatment of depression, suicidal attempts, and status epilepticus. Esketamine, which is ketamine formulated as a nasal spray, was approved by the Federal Drug Administration (FDA) in March 2019 as an adjuvant drug to treat treatment-resistant depression. NMDA receptor antagonists treat AD through offsetting AD-related pathological stimulation of subtypes of glutamate receptors in the central nervous system. Recent clinical findings suggest that ketamine may provide neuroprotection and reduce neuropsychiatric symptoms associated with AD. In the present investigation, we evaluate the potential role of ketamine and its postulated mechanism in AD management.
Recommended Citation
Mohammad Shehata, I.,
Masood, W.,
Nemr, N.,
Anderson, A.,
Bhusal, K.,
Edinoff, A. N.,
Cornett, E. M.,
Kaye, A. M.,
&
Kaye, A. D.
(2022).
The Possible Application of Ketamine in the Treatment of Depression in Alzheimer's Disease.
Neurology international, 14(2), 310–321.
DOI: 10.3390/neurolint14020025
https://scholarlycommons.pacific.edu/phs-facarticles/604
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This work is licensed under a Creative Commons Attribution 4.0 International License.