Newly Developed Drugs for Alzheimer’s Disease in Relation to Energy Metabolism, Cholinergic and Monoaminergic Neurotransmission
Abstract
Current options for Alzheimer's disease (AD) treatment are based on administration of cholinesterase inhibitors (donepezil, rivastigmine, galantamine) and/or memantine, acting as an N-methyl-D-aspartate (NMDA). Therapeutic approaches vary and include novel cholinesterase inhibitors, modulators of NMDA receptors, monoamine oxidase (MAO) inhibitors, immunotherapeutics, modulators of mitochondrial permeability transition pores (mPTP), amyloid-beta binding alcohol dehydrogenase (ABAD) modulators, antioxidant agents, etc. The novel trends of AD therapy are focused on multiple targeted ligands, where mostly ChE inhibition is combined with additional biological properties, positively affecting neuronal energy metabolism as well as mitochondrial functions, and possessing antioxidant properties. The present review summarizes newly developed drugs targeting cholinesterase and MAO, as well as drugs affecting mitochondrial functions.
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The contribution of acetylcholinesterase inhibitors is very insignificant in modifying properties that trigger Alzheimer's disease.
“its contribution is very insignificant in modifying properties that trigger AD”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [37]
The action of restoring cholinergic neuronal transmission by acetylcholinesterase inhibitors has been observed with a maximum in patients tolerant to the drug for 3 years.
“the action of restoring cholinergic neuronal transmission has been observed with a maximum in patients tolerant to the drug for 3 years”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [37]
In complementary therapies with acetylcholinesterase inhibitors, memantine's beneficial effects are observed, producing a decline in Alzheimer's disease; however, this condition is visible within a maximum period of 3 years, after which Alzheimer's disease continues to progress.
“In complementary therapies with AChEI, its beneficial effects are observed, producing a decline in AD; however, it has been reported that this condition is visible within a maximum period of 3 years, after which AD continues to progress [37].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [37]
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References 144 · Cited by 64
- Authors
- Korábečný, J., Nepovimová, E., Cikánková, T., Špilovská, K., Vašková, L., Mezeiová, E., Kuča, K., & Hroudová, J.
- Affiliations
- University Hospital Hradec Králové (CZ)
- Charles University (CZ)
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 370
- Pages
- 191-206
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2724309495
- Cited by
- 64
- References
- 144
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 7 · 2023: 6 · 2022: 8 · 2021: 7 · 2020: 16 · 2019: 7 · 2018: 7 · 2017: 2
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, cholinesterase inhibitors, monoamine oxidase inhibitors, mitochondrial bioenergetics, mitochondrial function, NMDA receptor modulators, cholinergic neurotransmission, monoaminergic neurotransmission, antioxidants, mitochondrial permeability transition pore, combination therapy
- MeSH terms
- Acetylcholine, Alzheimer Disease, Animals, Central Nervous System Agents, Energy Metabolism, Humans, Synaptic Transmission, Biogenic Monoamines
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