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Special Issue "Molecular Mechanisms of Alzheimer’s Disease and Brain Tolerance"

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 May 2021.

Special Issue Editor

Dr. Sónia C. Correia
E-Mail Website
Guest Editor
CNC - Center for Neuroscience and Cell Biology, University of Coimbra, Portugal
Interests: Alzheimer's disease; preconditioning; mitochondria; HIF-1alpha
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

It is well-known that Alzheimer’s disease (AD) is the main cause of dementia and the most prevalent brain disorder in the elderly, being considered a major public health concern worldwide. More than 100 years after the first case report, AD is still an incurable disease with no effective disease-modifying therapies, in part because the etiopathogenesis of this devastating neurogenerative disease remains elusive. In this sense, the Special Issue “Molecular Mechanisms of Alzheimer’s Disease and Brain Tolerance” aims to gather the most recent advances in the field to provide a more comprehensive picture of the molecular basis underlying the selective neuronal degeneration and loss in AD. Furthermore, this Special Issue also intends to describe the endogenous adaptative and pro-survival mechanisms behind brain tolerance (hormesis/conditioning) as promising targets to counteract AD symptomatology and neuropathology in a timely manner.

This Special Issue welcomes the submission of original research or review articles focusing on the cellular and molecular events that contribute to the onset and progression of AD (i.e., vascular dysfunction, brain hypometabolism, mitochondrial dysfunction and oxidative stress, synaptic failure, neuroinflammation, gut dysbiosis, among others) and to brain tolerance against injury.

Dr. Sónia C. Correia
Guest Editor

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 papers will be 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

  • Alzheimer’s disease
  • brain metabolism
  • endoplasmic reticulum
  • hormesis
  • microbiome
  • mitochondria
  • neuroinflammation
  • oxidative stress
  • synapses
  • vascular component

Published Papers (2 papers)

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Research

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Open AccessArticle
Key Disease Mechanisms Linked to Alzheimer’s Disease in the Entorhinal Cortex
Int. J. Mol. Sci. 2021, 22(8), 3915; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083915 - 10 Apr 2021
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Abstract
Alzheimer’s disease (AD) is a chronic, neurodegenerative brain disorder affecting millions of Americans that is expected to increase in incidence with the expanding aging population. Symptomatic AD patients show cognitive decline and often develop neuropsychiatric symptoms due to the accumulation of insoluble proteins [...] Read more.
Alzheimer’s disease (AD) is a chronic, neurodegenerative brain disorder affecting millions of Americans that is expected to increase in incidence with the expanding aging population. Symptomatic AD patients show cognitive decline and often develop neuropsychiatric symptoms due to the accumulation of insoluble proteins that produce plaques and tangles seen in the brain at autopsy. Unexpectedly, some clinically normal individuals also show AD pathology in the brain at autopsy (asymptomatic AD, AsymAD). In this study, SWItchMiner software was used to identify key switch genes in the brain’s entorhinal cortex that lead to the development of AD or disease resilience. Seventy-two switch genes were identified that are differentially expressed in AD patients compared to healthy controls. These genes are involved in inflammation, platelet activation, and phospholipase D and estrogen signaling. Peroxisome proliferator-activated receptor γ (PPARG), zinc-finger transcription factor (YY1), sterol regulatory element-binding transcription factor 2 (SREBF2), and early growth response 1 (EGR1) were identified as transcription factors that potentially regulate switch genes in AD. Comparing AD patients to AsymAD individuals revealed 51 switch genes; PPARG as a potential regulator of these genes, and platelet activation and phospholipase D as critical signaling pathways. Chemical–protein interaction analysis revealed that valproic acid is a therapeutic agent that could prevent AD from progressing. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Alzheimer’s Disease and Brain Tolerance)
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Review

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Open AccessReview
A Fundamental Role for Oxidants and Intracellular Calcium Signals in Alzheimer’s Pathogenesis—And How a Comprehensive Antioxidant Strategy May Aid Prevention of This Disorder
Int. J. Mol. Sci. 2021, 22(4), 2140; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042140 - 21 Feb 2021
Cited by 1 | Viewed by 654
Abstract
Oxidative stress and increased cytoplasmic calcium are key mediators of the detrimental effects on neuronal function and survival in Alzheimer’s disease (AD). Pathways whereby these perturbations arise, and then prevent dendritic spine formation, promote tau hyperphosphorylation, further amplify amyloid β generation, and induce [...] Read more.
Oxidative stress and increased cytoplasmic calcium are key mediators of the detrimental effects on neuronal function and survival in Alzheimer’s disease (AD). Pathways whereby these perturbations arise, and then prevent dendritic spine formation, promote tau hyperphosphorylation, further amplify amyloid β generation, and induce neuronal apoptosis, are described. A comprehensive program of nutraceutical supplementation, comprised of the NADPH oxidase inhibitor phycocyanobilin, phase two inducers, the mitochondrial antioxidant astaxanthin, and the glutathione precursor N-acetylcysteine, may have important potential for antagonizing the toxic effects of amyloid β on neurons and thereby aiding prevention of AD. Moreover, nutraceutical antioxidant strategies may oppose the adverse impact of amyloid β oligomers on astrocyte clearance of glutamate, and on the ability of brain capillaries to export amyloid β monomers/oligomers from the brain. Antioxidants, docosahexaenoic acid (DHA), and vitamin D, have potential for suppressing microglial production of interleukin-1β, which potentiates the neurotoxicity of amyloid β. Epidemiology suggests that a health-promoting lifestyle, incorporating a prudent diet, regular vigorous exercise, and other feasible measures, can cut the high risk for AD among the elderly by up to 60%. Conceivably, complementing such lifestyle measures with long-term adherence to the sort of nutraceutical regimen outlined here may drive down risk for AD even further. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Alzheimer’s Disease and Brain Tolerance)
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