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Special Issue "New Horizons for Amyloid Beta-Protein and Neurometabolism"

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A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 2881

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Special Issue Editors

Prof. Dr. Carlos Alberto Gonçalves

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Guest Editor

Laboratory of Calcium-Binding Proteins in the CNS, Departamento de Bioquímica, Universidade Federal of Rio Grande do Sul, Porto Alegre 90040-060, Brazil
Interests: astrocyte; Alzheimer; calcium-binding proteins; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Carla Inês Tasca

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Guest Editor

Laboratório de Neuroquímica-4, Departamento de Bioquímica, Universidade Federal de Santa Catarina, Florianopolis, Brazil
Interests: neurodegeneration; neuroprotection; glutamate; purinergic signaling

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is the main age-related neurodegenerative disease and is characterized by cognitive impairment and gradual damage in the function and structure of the hippocampus and cerebral cortex, two regions intimately related to memory and cognitive functioning. The neuropathologic hallmarks of AD include amyloid-beta (Aβ) formation and aggregation, and neurofibrillary tangles of hyperphosphorylated tau protein. Nevertheless, the early synaptic dysfunction in AD is associated with the oligomeric Aβ deposition and metabolic alterations, such as changes in glucose availability and metabolization pathways, endoplasmic reticulum and mitochondria dysfunction, oxidative stress and neuroinflammatory changes. It is essential that we know more about the metabolic changes that precede or accompany Aβ accumulation.

This Special Issue of Metabolites titled “New Horizons for Amyloid Beta-Protein and Neurometabolism” is dedicated to the evaluation of metabolic alterations associated with AD. Clinical, preclinical, imaging and bioinformatics studies concerning metabolomics analysis, cognitive assessment, bioenergetics, intermediate metabolites, endoplasmic reticulum stress, mitochondrial function/dysfunction, oxidative stress, biomarkers, neurotransmitters and signaling pathways are welcome. Additionally, manuscripts dealing with the identification of putative neuroprotective strategies and their effects on neurometabolism are also highly desired.

Prof. Dr. Carlos Alberto Gonçalves
Prof. Dr. Carla Inês Tasca
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. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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
amyloid-beta production
amyloid-beta clearance
metabolites
ER stress
bioenergetics
oxidative stress
mitochondrial dysfunction
neuroinflammation
biomarkers
neuroprotection

Published Papers (3 papers)

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Research

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Open AccessArticle

Guanosine Prevents Spatial Memory Impairment and Hippocampal Damage Following Amyloid-β_1–42 Administration in Mice

Victor Coelho

Luisa Bandeira Binder

Naiani Ferreira Marques

Leandra Celso Constantino

Gianni Mancini

and

Carla Inês Tasca

Metabolites 2022, 12(12), 1207; https://doi.org/10.3390/metabo12121207 - 01 Dec 2022

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Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative illness responsible for cognitive impairment and dementia. Accumulation of amyloid-beta (Aβ) peptides in neurons and synapses causes cell metabolism to unbalance, and the production of reactive oxygen species (ROS), leading to neuronal death and cognitive damage. Guanosine is an endogenous nucleoside recognized as a neuroprotective agent since it prevents glutamate-induced neurotoxicity by a mechanism not yet completely elucidated. In this study, we evaluated behavioral and biochemical effects in the hippocampus caused by the intracerebroventricular (i.c.v.) infusion of Aβ_1–42 peptide (400 pmol/site) in mice, and the neuroprotective effect of guanosine (8 mg/kg, i.p.). An initial evaluation on the eighth day after Aβ_1–42 infusion showed no changes in the tail suspension test, although ex vivo analyses in hippocampal slices showed increased ROS production. In the second protocol, on the tenth day following Aβ_1–42 infusion, no effect was observed in the sucrose splash test, but a reduction in the recognition index in the object location test showed impaired spatial memory. Analysis of hippocampal slices showed no ROS production and mitochondrial membrane potential alteration, but a tendency to increase glutamate release and a significant lactate release, pointing to a metabolic alteration. Those effects were accompanied by decreased cell viability and increased membrane damage. Guanosine treatment prevented behavioral and biochemical alterations evoked by Aβ_1–42, suggesting a potential role against behavioral and biochemical damage evoked by Aβ in the hippocampus. Full article

(This article belongs to the Special Issue New Horizons for Amyloid Beta-Protein and Neurometabolism)

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Open AccessArticle

LC-MS/MS Insight into Vitamin C Restoration to Metabolic Disorder Evoked by Amyloid β in Caenorhabditis elegans CL2006

and

Metabolites 2022, 12(9), 841; https://doi.org/10.3390/metabo12090841 - 06 Sep 2022

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Abstract

The transitional expression and aggregation of amyloid β (Aβ) are the most important causative factors leading to the deterioration of Alzheimer’s disease (AD), a commonly occurring metabolic disease among older people. Antioxidant agents such as vitamin C (Vc) have shown potential effects against AD and aging. We applied an liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) method and differential metabolites strategy to explore the metabolic disorders and Vc restoration in a human Aβ transgenic (Punc-54::Aβ^1–42) nematode model CL2006. We combined the LC-MS/MS investigation with the KEGG and HMDB databases and the CFM-ID machine-learning model to identify and qualify the metabolites with important physiological roles. The differential metabolites responding to Aβ activation and Vc treatment were filtered out and submitted to enrichment analysis. The enrichment showed that Aβ mainly caused abnormal biosynthesis and metabolism pathways of phenylalanine, tyrosine and tryptophan biosynthesis, as well as arginine and proline metabolism. Vc reversed the abnormally changed metabolites tryptophan, anthranilate, indole and indole-3-acetaldehyde. Vc restoration affected the tryptophan metabolism and the biosynthesis of phenylalanine, tyrosine and tryptophan. Our findings provide supporting evidence for understanding the metabolic abnormalities in neurodegenerative diseases and the repairing effect of drug interventions. Full article

(This article belongs to the Special Issue New Horizons for Amyloid Beta-Protein and Neurometabolism)

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Other

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Open AccessPerspective

SARS-CoV-2-Induced Amyloidgenesis: Not One, but Three Hypotheses for Cerebral COVID-19 Outcomes

Carlos-Alberto Gonçalves

Larissa Daniele Bobermin

Patricia Sesterheim

and

Carlos Alexandre Netto

Metabolites 2022, 12(11), 1099; https://doi.org/10.3390/metabo12111099 - 11 Nov 2022

Viewed by 854

Abstract

The main neuropathological feature of Alzheimer’s disease (AD) is extracellular amyloid deposition in senile plaques, resulting from an imbalance between the production and clearance of amyloid beta peptides. Amyloid deposition is also found around cerebral blood vessels, termed cerebral amyloid angiopathy (CAA), in 90% of AD cases. Although the relationship between these two amyloid disorders is obvious, this does not make CAA a characteristic of AD, as 40% of the non-demented population presents this derangement. AD is predominantly sporadic; therefore, many factors contribute to its genesis. Herein, the starting point for discussion is the COVID-19 pandemic that we are experiencing and how SARS-CoV-2 may be able to, both directly and indirectly, contribute to CAA, with consequences for the outcome and extent of the disease. We highlight the role of astrocytes and endothelial cells in the process of amyloidgenesis, as well as the role of other amyloidgenic proteins, such as fibrinogen and serum amyloid A protein, in addition to the neuronal amyloid precursor protein. We discuss three independent hypotheses that complement each other to explain the cerebrovascular amyloidgenesis that may underlie long-term COVID-19 and new cases of dementia. Full article

(This article belongs to the Special Issue New Horizons for Amyloid Beta-Protein and Neurometabolism)

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