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Intersection between Cognitive Impairment and Metabolic Alterations in the Molecular Mechanisms of Neurodegeneration

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: closed (31 March 2023) | Viewed by 9245

Special Issue Editors

Dr. Agueda A. Rostagno

E-Mail Website
Guest Editor
NYU, Department of Pathology, Grossman School of Medicine, 550 First Avenue, New York, NY 10016, USA
Interests: Alzheimer's disease; amyloidosis; neurodegenerative disorders, autophagy; apoptosis; mitochondrial dysfunction; oxidative stress; metabolic dysregulation; cerebral amyloid angiopathy; molecular chaperones; immunohistochemistry; neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Jorge Ghiso

E-Mail Website
Guest Editor
Department of Pathology, Grossman School of Medicine, New York University, New York, NY 10016, USA
Interests: Alzheimer disease; neurodegenerative disorders; systemic and cerebral amyloidoses; aging; proteomics; post-translational modifications; blood-brain-barrier; amyloid; neurofibrillary tangles; cerebral amyloid angiopathy; cerebral hemorrhage; translational approaches; mouse models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

In recent decades, the incidence of neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases, vascular dementia, amyotrophic lateral sclerosis, and Huntington's disease, among others, has tremendously increased worldwide. Despite extensive research, the complex molecular mechanisms driving the pathogenesis of these disorders have not been fully elucidated, and disease-modifying therapeutic strategies remain to be discovered. Among the different pathways compromising the diverse group of neurodegenerative diseases, mounting evidence highlights a central role for mitochondrial detrimental changes, an altered cerebral glucose metabolism, and metabolic/bioenergetic shifts that frequently precede the cognitive abnormalities.

In parallel, cognitive dysfunction is being progressively recognized as a major comorbidity of metabolic diseases, particularly diabetes mellitus, and is often associated with metabolic stressors as the consumption of high-fat content diets and sedentary life styles. Experimental and epidemiological evidence suggests that the same molecular pathways implicated in insulin resistance, mitochondrial dysfunction, apoptosis, inflammation, and oxidative stress play a link between metabolism and cognitive dysfunction, suggesting causal relationships between different possible molecular etiologic factors.

This Special Issue aims to provide insight into the interplay between the multifaceted molecular pathways linking metabolic/bioenergetic alterations as significant contributors to the synaptic alterations, neuroinflammatory mechanisms, vascular dysfunction, and cognitive impairment associated with neurodegeneration. We welcome contributions in the form of original research articles, reviews and communications.

Dr. Agueda A. Rostagno
Prof. Dr. Jorge Ghiso
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • cognitive impairment
  • neurodegeneration
  • vascular dysfunction
  • neuroinflammatory
  • cognitive abnormalities

Related Special Issue

Published Papers (3 papers)

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Research

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16 pages, 1302 KiB  
Article
Association of NGF and Mitochondrial Respiration with Autism Spectrum Disorder
by Maria Gevezova, Danail Minchev, Iliana Pacheva, Tatyana Todorova, Ralitsa Yordanova, Elena Timova, Ivan Ivanov and Victoria Sarafian
Int. J. Mol. Sci. 2022, 23(19), 11917; https://doi.org/10.3390/ijms231911917 - 7 Oct 2022
Cited by 6 | Viewed by 1789
Abstract
Background: NGF is a molecule with a pleiotropic role, affecting neuro-immune functions, energy homeostasis, and synaptic plasticity. The mechanisms of NGF-induced neuronal differentiation are well established, but its effect on mitochondria in autism spectrum disorder (ASD) is still unclear. We hypothesize that NGF-induced [...] Read more.
Background: NGF is a molecule with a pleiotropic role, affecting neuro-immune functions, energy homeostasis, and synaptic plasticity. The mechanisms of NGF-induced neuronal differentiation are well established, but its effect on mitochondria in autism spectrum disorder (ASD) is still unclear. We hypothesize that NGF-induced neuronal development requires large amounts of energy, and mitochondria in ASD are overloaded to meet the new functional requirements. Method: The study includes primary diagnosed ASD children. Peripheral blood mononuclear cells (PBMCs) and plasma were obtained from both patients and typically developing children (TDC). PBMCs were analyzed with Seahorse XFp, and plasma NGF protein levels were measured. Results: We detected nearly 50% higher NGF levels and approximately 40% elevation in spare respiratory capacity in ASD compared to TDC. These findings are consistent with the observed difference in maximal respiration, which was also significantly higher in the patient group. Both mitochondrial respiration and NGF plasma levels exhibit a strong potential to discriminate children with ASD from TDC. Conclusions: This study is the first to link elevated NGF with mitochondrial respiration and altered energy homeostasis in ASD. High NGF correlates with basic bioenergetic signatures that may be used as a screening tool to improve early diagnosis and clinical follow-up in ASD. Full article
(This article belongs to the Special Issue Intersection between Cognitive Impairment and Metabolic Alterations in the Molecular Mechanisms of Neurodegeneration)
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16 pages, 3234 KiB  
Article
Therapeutic Effect of Erythropoietin on Alzheimer’s Disease by Activating the Serotonin Pathway
by Kyu-Ho Shim, Sungchan Ha, Jin Seung Choung, Jee In Choi, Daniel Youngsuk Kim, Jong Moon Kim and MinYoung Kim
Int. J. Mol. Sci. 2022, 23(15), 8144; https://doi.org/10.3390/ijms23158144 - 24 Jul 2022
Cited by 1 | Viewed by 2295
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by memory impairment in patients. Erythropoietin (EPO) has been reported to stimulate neurogenesis. This study was conducted to determine the regenerative effects of EPO in an AD model and to assess its underlying mechanism. Recombinant [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by memory impairment in patients. Erythropoietin (EPO) has been reported to stimulate neurogenesis. This study was conducted to determine the regenerative effects of EPO in an AD model and to assess its underlying mechanism. Recombinant human EPO was intraperitoneally administered to AD mice induced by intracerebroventricular Aβ oligomer injection. Behavioral assessments with novel object recognition test and passive avoidance task showed improvement in memory function of the EPO-treated AD mice compared to that of the saline-treated AD mice (p < 0.0001). An in vivo protein assay for the hippocampus and cortex tissue indicated that EPO treatment modulated neurotransmitters, including dopamine, serotonin, and adrenaline. EPO treatment also restored the activity of serotonin receptors, including 5-HT4R, 5-HT7R, and 5-HT1aR (p < 0.01), at mRNA levels. Furthermore, EPO seemed to exert an anti-inflammatory influence by downregulating TLR4 at mRNA and protein levels (p < 0.05). Finally, an immunohistochemical assay revealed increments of Nestin(+) and NeuN(+) neuronal cells in the CA3 region in the EPO-treated AD mice compared to those in the saline-treated AD mice. The conclusion is that EPO administration might be therapeutic for AD by activating the serotonergic pathway, anti-inflammatory action, and neurogenic characteristics. Full article
(This article belongs to the Special Issue Intersection between Cognitive Impairment and Metabolic Alterations in the Molecular Mechanisms of Neurodegeneration)
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Review

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26 pages, 761 KiB  
Review
Protein Misfolding and Aggregation in the Brain: Common Pathogenetic Pathways in Neurodegenerative and Mental Disorders
by Aleksandra Ochneva, Yana Zorkina, Olga Abramova, Olga Pavlova, Valeriya Ushakova, Anna Morozova, Eugene Zubkov, Konstantin Pavlov, Olga Gurina and Vladimir Chekhonin
Int. J. Mol. Sci. 2022, 23(22), 14498; https://doi.org/10.3390/ijms232214498 - 21 Nov 2022
Cited by 7 | Viewed by 4454
Abstract
Mental disorders represent common brain diseases characterized by substantial impairments of social and cognitive functions. The neurobiological causes and mechanisms of psychopathologies still have not been definitively determined. Various forms of brain proteinopathies, which include a disruption of protein conformations and the formation [...] Read more.
Mental disorders represent common brain diseases characterized by substantial impairments of social and cognitive functions. The neurobiological causes and mechanisms of psychopathologies still have not been definitively determined. Various forms of brain proteinopathies, which include a disruption of protein conformations and the formation of protein aggregates in brain tissues, may be a possible cause behind the development of psychiatric disorders. Proteinopathies are known to be the main cause of neurodegeneration, but much less attention is given to the role of protein impairments in psychiatric disorders’ pathogenesis, such as depression and schizophrenia. For this reason, the aim of this review was to discuss the potential contribution of protein illnesses in the development of psychopathologies. The first part of the review describes the possible mechanisms of disruption to protein folding and aggregation in the cell: endoplasmic reticulum stress, dysfunction of chaperone proteins, altered mitochondrial function, and impaired autophagy processes. The second part of the review addresses the known proteins whose aggregation in brain tissue has been observed in psychiatric disorders (amyloid, tau protein, α-synuclein, DISC-1, disbindin-1, CRMP1, SNAP25, TRIOBP, NPAS3, GluA1, FABP, and ankyrin-G). Full article
(This article belongs to the Special Issue Intersection between Cognitive Impairment and Metabolic Alterations in the Molecular Mechanisms of Neurodegeneration)
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