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Special Issue "The Involvement of Cholinergic and Norepinephrine Network Modulation in Alzheimer’s Disease Cognitive Dysfunction"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 October 2021.

Special Issue Editors

Dr. Noriyuki Matsukawa
E-Mail Website
Guest Editor
Department of Neurology, Nagoya City University Graduate School of Medicine, Nagoya, Japan
Interests: Clinical Neurology; Alzheimer’s disease; Parkinson disease; Parkinson-related disease; Cognitive dysfunction; Neurobiology; Neurophysiology; Neuroprotection; Neurorehabilitation; Neuroradiology
Dr. Daisuke Kato
E-Mail
Guest Editor
Department of Anatomy and Molecular Cell Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan
Interests: Neurophysiology; Neurobiology; Molecular biology; Oligodendrocyte; Microglia; Neural network; Clinical Neurology

Special Issue Information

Dear Colleagues,

Some people can tolerate more Alzheimer’s-related pathological change, senile plagues, and neurofibrillary tangles than others, due to having a “cognitive reserve.” In individuals with cognitive reserve, the functional network connection in the cerebral cortex can be visualized as intact using functional Magnetic Resonance Imaging. However, the details of the molecular mechanism underlying the prevention of cognitive impairment in the presence of AD-related pathology are still unknown. Interestingly, the cholinergic and/or adrenergic neural signaling may modulate hippocampal glutamatergic neural activity under the AD-related pathology. In this Special Issue, we are seeking novel research and/or review articles on:

  • The pathological condition and cognitive dysfunction
  • The advancement of AD model animal from a standpoint of neural network
  • Neurophysiological network and/or modulation
  • Prevention of impairment in cognition/neural network under AD-related pathology
  • Functional Magnetic Resonance Imaging and neural network

In this issue, we are looking for articles clearly articulating the molecular and/or physiological mechanism underlying cognitive reserve in patients with AD-related pathology.

Dr. Noriyuki Matsukawa
Dr. Daisuke Kato
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Alzheimer’s disease
  • Cognitive dysfunction
  • Neural modulation
  • Cholinergic neural signaling
  • Norepinephrine neural signaling
  • Neurophysiology
  • Neurobiology
  • Functional imaging
  • Rehabilitation

Published Papers (3 papers)

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Review

Open AccessReview
Involvement of Cholinergic, Adrenergic, and Glutamatergic Network Modulation with Cognitive Dysfunction in Alzheimer’s Disease
Int. J. Mol. Sci. 2021, 22(5), 2283; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052283 - 25 Feb 2021
Viewed by 421
Abstract
Alzheimer’s disease (AD), the most common cause of dementia, is a progressive neurodegenerative disease. The number of AD cases has been rapidly growing worldwide. Several the related etiological hypotheses include atypical amyloid β (Aβ) deposition, neurofibrillary tangles of tau proteins inside neurons, disturbed [...] Read more.
Alzheimer’s disease (AD), the most common cause of dementia, is a progressive neurodegenerative disease. The number of AD cases has been rapidly growing worldwide. Several the related etiological hypotheses include atypical amyloid β (Aβ) deposition, neurofibrillary tangles of tau proteins inside neurons, disturbed neurotransmission, inflammation, and oxidative stress. During AD progression, aberrations in neurotransmission cause cognitive decline—the main symptom of AD. Here, we review the aberrant neurotransmission systems, including cholinergic, adrenergic, and glutamatergic network, and the interactions among these systems as they pertain to AD. We also discuss the key role of N-methyl-d-aspartate receptor (NMDAR) dysfunction in AD-associated cognitive impairment. Furthermore, we summarize the results of recent studies indicating that increasing glutamatergic neurotransmission through the alteration of NMDARs shows potential for treating cognitive decline in mild cognitive impairment or early stage AD. Future studies on the long-term efficiency of NMDA-enhancing strategies in the treatment of AD are warranted. Full article
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Open AccessReview
The Role of Butyrylcholinesterase and Iron in the Regulation of Cholinergic Network and Cognitive Dysfunction in Alzheimer’s Disease Pathogenesis
Int. J. Mol. Sci. 2021, 22(4), 2033; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042033 - 18 Feb 2021
Viewed by 1017
Abstract
Alzheimer’s disease (AD), the most common form of dementia in elderly individuals, is marked by progressive neuron loss. Despite more than 100 years of research on AD, there is still no treatment to cure or prevent the disease. High levels of amyloid-β (Aβ) [...] Read more.
Alzheimer’s disease (AD), the most common form of dementia in elderly individuals, is marked by progressive neuron loss. Despite more than 100 years of research on AD, there is still no treatment to cure or prevent the disease. High levels of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs) in the brain are neuropathological hallmarks of AD. However, based on postmortem analyses, up to 44% of individuals have been shown to have high Aβ deposits with no clinical signs, due to having a “cognitive reserve”. The biochemical mechanism explaining the prevention of cognitive impairment in the presence of Aβ plaques is still unknown. It seems that in addition to protein aggregation, neuroinflammatory changes associated with aging are present in AD brains that are correlated with a higher level of brain iron and oxidative stress. It has been shown that iron accumulates around amyloid plaques in AD mouse models and postmortem brain tissues of AD patients. Iron is required for essential brain functions, including oxidative metabolism, myelination, and neurotransmitter synthesis. However, an imbalance in brain iron homeostasis caused by aging underlies many neurodegenerative diseases. It has been proposed that high iron levels trigger an avalanche of events that push the progress of the disease, accelerating cognitive decline. Patients with increased amyloid plaques and iron are highly likely to develop dementia. Our observations indicate that the butyrylcholinesterase (BChE) level seems to be iron-dependent, and reports show that BChE produced by reactive astrocytes can make cognitive functions worse by accelerating the decay of acetylcholine in aging brains. Why, even when there is a genetic risk, do symptoms of the disease appear after many years? Here, we discuss the relationship between genetic factors, age-dependent iron tissue accumulation, and inflammation, focusing on AD. Full article
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Open AccessReview
The Cholinergic System, the Adrenergic System and the Neuropathology of Alzheimer’s Disease
Int. J. Mol. Sci. 2021, 22(3), 1273; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031273 - 28 Jan 2021
Cited by 2 | Viewed by 722
Abstract
Neurodegenerative diseases are a major public health problem worldwide with a wide spectrum of symptoms and physiological effects. It has been long reported that the dysregulation of the cholinergic system and the adrenergic system are linked to the etiology of Alzheimer’s disease. Cholinergic [...] Read more.
Neurodegenerative diseases are a major public health problem worldwide with a wide spectrum of symptoms and physiological effects. It has been long reported that the dysregulation of the cholinergic system and the adrenergic system are linked to the etiology of Alzheimer’s disease. Cholinergic neurons are widely distributed in brain regions that play a role in cognitive functions and normal cholinergic signaling related to learning and memory is dependent on acetylcholine. The Locus Coeruleus norepinephrine (LC-NE) is the main noradrenergic nucleus that projects and supplies norepinephrine to different brain regions. Norepinephrine has been shown to be neuroprotective against neurodegeneration and plays a role in behavior and cognition. Cholinergic and adrenergic signaling are dysregulated in Alzheimer’s disease. The degeneration of cholinergic neurons in nucleus basalis of Meynert in the basal forebrain and the degeneration of LC-NE neurons were reported in Alzheimer’s disease. The aim of this review is to describe current literature on the role of the cholinergic system and the adrenergic system (LC-NE) in the pathology of Alzheimer’s disease and potential therapeutic implications. Full article
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