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Cells
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Molecular and Cellular Basis of Alzheimer's Disease
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Molecular and Cellular Basis of Alzheimer's Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 3794

Special Issue Editors

Dr. Xavier Gallart-Palau

E-Mail Website
Guest Editor
1. Institut d'Investigació Sanitària Pere Virgili (IISPV), Reus, Spain
2. Carlos III Health Institute (Instituto de Salud Carlos III), Madrid, Spain
Interests: neurochemistry; proteinopathy; Alzheimer’s disease; vascular dementia; neurovascular unit; extracellular vesicles; proteomics
Special Issues, Collections and Topics in MDPI journals
Dr. Aida Serra

E-Mail Website
Guest Editor
1. IMDEA Food & Health Sciences Research Institute, +Pec Proteomics, Campus of International Excellence UAM+CSIC, Old Cantoblanco Hospital, 8 Crta. Canto Blanco, 28049 Madrid, Spain
2. Proteored-Instituto de Salud Carlos III (ISCIII), Madrid, Spain
Interests: proteomics; neurodegeneration; extracellular vesicles; protein post-translational modifications; degenerative protein modifications; metabolism; human diseases
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Giulio Pasinetti

E-Mail Website
Guest Editor
Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: inflammation; inflammasome; beta-amyloid; Tau; microglia; apoptosis; caspase; Alzheimer’s disease; Parkinson’s disease; amyotrophic lateral sclerosis; frontotemporal dementia; traumatic brain injury; polyphenols; bioavailability; drug discovery
Special Issues, Collections and Topics in MDPI journals
Dr. Joyce Harary

E-Mail
Guest Editor
Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: Alzheimer’s Disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Alzheimer’s disease (AD) is the main contributor to dementia worldwide, a cognitive syndrome that progressively and fatally impairs the ability of the affected individuals to perform essential everyday tasks. Dementia is also the major cause of disability among elderly people worldwide, and its derived social and economic costs are massive. Although the molecular and cellular basis of AD remains a matter of intense scientific investigation and has been partially uncovered, several crucial aspects related to the neuropathology of AD still require our attention and interest. These aspects, although not exhaustive, may involve the following actions: uncovering currently unknown idiopathic triggering factors, shedding light on the molecular mechanisms of neuropathology onset, understanding common neuropathological mechanisms that defy brain cell heterogeneity, identifying potential early-onset biological diagnostic and prognostic markers (neuropathology onset proposed as early as 20 years before clinical diagnosis). Thus, this Special Issue focuses on generating genuine and valuable scientific knowledge on the molecular and cellular basis of AD, with foresight on the apparition of novel diagnosis and therapeutic strategies for this fatal neurological disorder.

You may choose our Joint Special Issue in Biomolecules, or Joint Special Issue in NeuroSci.

Dr. Xavier Gallart-Palau
Dr. Aida Serra
Prof. Dr. Giulio Pasinetti
Dr. Joyce Harary
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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.

Published Papers (1 paper)

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Research

15 pages, 4588 KiB  
Article
Beta-Amyloid Instigates Dysfunction of Mitochondria in Cardiac Cells
by Sehwan Jang, Xavier R. Chapa-Dubocq, Rebecca M. Parodi-Rullán, Silvia Fossati and Sabzali Javadov
Cells 2022, 11(3), 373; https://doi.org/10.3390/cells11030373 - 22 Jan 2022
Cited by 13 | Viewed by 2957
Abstract
Alzheimer’s disease (AD) includes the formation of extracellular deposits comprising aggregated β-amyloid (Aβ) fibers associated with oxidative stress, inflammation, mitochondrial abnormalities, and neuronal loss. There is an associative link between AD and cardiac diseases; however, the mechanisms underlying the potential role of AD, [...] Read more.
Alzheimer’s disease (AD) includes the formation of extracellular deposits comprising aggregated β-amyloid (Aβ) fibers associated with oxidative stress, inflammation, mitochondrial abnormalities, and neuronal loss. There is an associative link between AD and cardiac diseases; however, the mechanisms underlying the potential role of AD, particularly Aβ in cardiac cells, remain unknown. Here, we investigated the role of mitochondria in mediating the effects of Aβ1-40 and Aβ1-42 in cultured cardiomyocytes and primary coronary endothelial cells. Our results demonstrated that Aβ1-40 and Aβ1-42 are differently accumulated in cardiomyocytes and coronary endothelial cells. Aβ1-42 had more adverse effects than Aβ1-40 on cell viability and mitochondrial function in both types of cells. Mitochondrial and cellular ROS were significantly increased, whereas mitochondrial membrane potential and calcium retention capacity decreased in both types of cells in response to Aβ1-42. Mitochondrial dysfunction induced by Aβ was associated with apoptosis of the cells. The effects of Aβ1-42 on mitochondria and cell death were more evident in coronary endothelial cells. In addition, Aβ1-40 and Aβ1-42 significantly increased Ca2+ -induced swelling in mitochondria isolated from the intact rat hearts. In conclusion, this study demonstrates the toxic effects of Aβ on cell survival and mitochondria function in cardiac cells. Full article
(This article belongs to the Special Issue Molecular and Cellular Basis of Alzheimer's Disease)
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