Nicotinic acetylcholine receptors and learning and memory deficits in Neuroinflammatory diseases

Nicotinic acetylcholine receptors and learning and memory deficits in Neuroinflammatory diseases

Animal survival depends on cognitive abilities such as learning and memory to adapt to environmental changes. Memory functions require an enhanced activity and connectivity of a particular arrangement of engram neurons, supported by the concerted action of neurons, glia, and vascular cells. The dete...

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Published in:Frontiers in neuroscience Vol. 17; p. 1179611
Main Authors: Echeverria, Valentina, Mendoza, Cristhian, Iarkov, Alex
Format: Journal Article
Language:English
Published: Switzerland Frontiers Research Foundation 15-05-2023
Frontiers Media S.A
Subjects:
Acetylcholine receptors (nicotinic)
Aging
Alzheimer's disease
Brain
Cholinergic transmission
Cognitive ability
Cotinine
Dendritic cells
Endothelial cells
Environmental changes
Hypotheses
Inflammation
Interneurons
Learning
learning and memory
Memory
Movement disorders
Neural networks
Neurodegenerative diseases
Neurogenesis
Neurological diseases
Neuronal-glial interactions
Neurons
Neuroscience
Neurotransmission
nicotinic acetylcholine receptors
Older people
Parkinson's disease
Post traumatic stress disorder
posttraumatic stress disorder
Toll-like receptors
Traumatic brain injury
γ-Aminobutyric acid
learning and memory
cotinine
neurogenesis
traumatic brain injury
aging
nicotinic acetylcholine receptors
posttraumatic stress disorder
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Abstract Animal survival depends on cognitive abilities such as learning and memory to adapt to environmental changes. Memory functions require an enhanced activity and connectivity of a particular arrangement of engram neurons, supported by the concerted action of neurons, glia, and vascular cells. The deterioration of the cholinergic system is a common occurrence in neurological conditions exacerbated by aging such as traumatic brain injury (TBI), posttraumatic stress disorder (PTSD), Alzheimer's disease (AD), and Parkinson's disease (PD). Cotinine is a cholinergic modulator with neuroprotective, antidepressant, anti-inflammatory, antioxidant, and memory-enhancing effects. Current evidence suggests Cotinine's beneficial effects on cognition results from the positive modulation of the α7-nicotinic acetylcholine receptors (nAChRs) and the inhibition of the toll-like receptors (TLRs). The α7nAChR affects brain functions by modulating the function of neurons, glia, endothelial, immune, and dendritic cells and regulates inhibitory and excitatory neurotransmission throughout the GABA interneurons. In addition, Cotinine acting on the α7 nAChRs and TLR reduces neuroinflammation by inhibiting the release of pro-inflammatory cytokines by the immune cells. Also, α7nAChRs stimulate signaling pathways supporting structural, biochemical, electrochemical, and cellular changes in the Central nervous system during the cognitive processes, including Neurogenesis. Here, the mechanisms of memory formation as well as potential mechanisms of action of Cotinine on memory preservation in aging and neurological diseases are discussed.
AbstractList Animal survival depends on cognitive abilities such as learning and memory to adapt to environmental changes. Memory functions require an enhanced activity and connectivity of a particular arrangement of engram neurons, supported by the concerted action of neurons, glia, and vascular cells. The deterioration of the cholinergic system is a common occurrence in neurological conditions exacerbated by aging such as traumatic brain injury (TBI), posttraumatic stress disorder (PTSD), Alzheimer’s disease (AD), and Parkinson’s disease (PD). Cotinine is a cholinergic modulator with neuroprotective, antidepressant, anti-inflammatory, antioxidant, and memory-enhancing effects. Current evidence suggests Cotinine’s beneficial effects on cognition results from the positive modulation of the α7-nicotinic acetylcholine receptors (nAChRs) and the inhibition of the toll-like receptors (TLRs). The α7nAChR affects brain functions by modulating the function of neurons, glia, endothelial, immune, and dendritic cells and regulates inhibitory and excitatory neurotransmission throughout the GABA interneurons. In addition, Cotinine acting on the α7 nAChRs and TLR reduces neuroinflammation by inhibiting the release of pro-inflammatory cytokines by the immune cells. Also, α7nAChRs stimulate signaling pathways supporting structural, biochemical, electrochemical, and cellular changes in the Central nervous system during the cognitive processes, including Neurogenesis. Here, the mechanisms of memory formation as well as potential mechanisms of action of Cotinine on memory preservation in aging and neurological diseases are discussed.
Animal survival depends on cognitive abilities such as learning and memory to adapt to environmental changes. Memory functions require an enhanced activity and connectivity of a particular arrangement of engram neurons, supported by the concerted action of neurons, glia, and vascular cells. The deterioration of the cholinergic system is a common occurrence in several neurological disorders exacerbated by aging, such as traumatic brain injury (TBI), Posttraumatic stress disorder (PTSD), Alzheimer's disease (AD), and Parkinson's disease (PD). Cotinine is a drug with neuroprotector, antidepressant, anti-inflammatory, antioxidant, and memory enhancing effects[1]. Current evidence suggests that its beneficial effects on cognition results from the positive modulation of the α7-nicotinic acetylcholine receptors (nAChRs) and the inhibition of the toll like receptors (TLRs)[2]. The nAChRs affect brain functions by modulating neurons, glia, endothelial cells, immune cells, and dendritic cells and controlling inhibitory and excitatory neurotransmission through the GABA interneurons. In addition, the positive modulation of the α7nAChRs by Cotinine reduced neuroinflammation and the release of pro-inflammatory cytokines by immune cells. Also, α7nAChRs stimulate signaling pathways supporting the structural, biochemical, electrochemical, and cellular changes during the cognitive processes, including Neurogenesis. Here, potential mechanisms of action of Cotinine on memory preservation in aging and neurological diseases are discussed. Keywords: nicotinic acetylcholine receptors, learning and memory, aging, Cotinine, Neurogenesis, Posttraumatic stress disorder, traumatic brain injury
Author Echeverria, Valentina
Iarkov, Alex
Mendoza, Cristhian
AuthorAffiliation 2 Research and Development Department, Bay Pines VAHCS , Bay Pines, FL , United States
1 Facultad de Medicina y Ciencia, Universidad San Sebastián , Concepción , Chile
3 Facultad de Odontologia y Ciencias de la Rehabilitacion, Universidad San Sebastián , Concepción , Chile
AuthorAffiliation_xml – name: 3 Facultad de Odontologia y Ciencias de la Rehabilitacion, Universidad San Sebastián , Concepción , Chile
– name: 2 Research and Development Department, Bay Pines VAHCS , Bay Pines, FL , United States
– name: 1 Facultad de Medicina y Ciencia, Universidad San Sebastián , Concepción , Chile
Author_xml – sequence: 1
  givenname: Valentina
  surname: Echeverria
  fullname: Echeverria, Valentina
  organization: Research and Development Department, Bay Pines VAHCS, Bay Pines, FL, United States
– sequence: 2
  givenname: Cristhian
  surname: Mendoza
  fullname: Mendoza, Cristhian
  organization: Facultad de Odontologia y Ciencias de la Rehabilitacion, Universidad San Sebastián, Concepción, Chile
– sequence: 3
  givenname: Alex
  surname: Iarkov
  fullname: Iarkov, Alex
  organization: Facultad de Medicina y Ciencia, Universidad San Sebastián, Concepción, Chile
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37255751$$D View this record in MEDLINE/PubMed
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2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright © 2023 Echeverria, Mendoza and Iarkov. 2023 Echeverria, Mendoza and Iarkov
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Keywords learning and memory
cotinine
neurogenesis
traumatic brain injury
aging
nicotinic acetylcholine receptors
posttraumatic stress disorder
Language English
License Copyright © 2023 Echeverria, Mendoza and Iarkov.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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SubjectTerms Acetylcholine receptors (nicotinic)
Aging
Alzheimer's disease
Brain
Cholinergic transmission
Cognitive ability
Cotinine
Dendritic cells
Endothelial cells
Environmental changes
Hypotheses
Inflammation
Interneurons
Learning
learning and memory
Memory
Movement disorders
Neural networks
Neurodegenerative diseases
Neurogenesis
Neurological diseases
Neuronal-glial interactions
Neurons
Neuroscience
Neurotransmission
nicotinic acetylcholine receptors
Older people
Parkinson's disease
Post traumatic stress disorder
posttraumatic stress disorder
Toll-like receptors
Traumatic brain injury
γ-Aminobutyric acid
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Title Nicotinic acetylcholine receptors and learning and memory deficits in Neuroinflammatory diseases
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