molecules-logo

Journal Browser

Journal Browser

Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease—Second Edition

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 1444

Special Issue Editors


E-Mail Website
Guest Editor
1. Faculty of Pharmacy, Lithuanian University of Health Sciences, Kaunas, Lithuania
2. Neuroscience Institute, Lithuanian University of Health Sciences, Kaunas, Lithuania
Interests: cell death; energy metabolism; mitochondria; inflammation; neurodegenerative disorders; ischemia/reperfusion; amyloid proteins; brain cell cultures
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Faculty of Pharmacy, Lithuanian University of Health Sciences, Kaunas, Lithuania
Interests: protective and toxic mechanisms of bioactive compounds; ischemia; anoxia; stress conditions; cellular energy turnover; mitochondrial functions; ion channels; computer modeling in drug discovery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The world’s population is aging. Aging is the primary risk factor for most neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, etc. In addition, aging is the strongest risk factor for ischemic stroke, and brain ischemia could progress and lead to the development of neurodegeneration. Both pathologies are life-threatening and may cause death or severe complications. Consequently, new therapies are constantly being sought out and one of the research directions is a search for effective neuroprotective agents. Oxidative stress, mitochondrial injury, and inflammation activation leading to brain cell death have been suggested as key mechanisms of irreversible damage in many neurological disorders. The accumulation of several oxidation products in neurons during aging and pathological conditions supports the idea that the presence of natural antioxidant biomolecules may be a beneficial alternative therapy for neurodegeneration and other related diseases. Consequently, mitochondria-targeted or inflammatory response-regulated bioactive compounds may be promising candidate therapeutics for the prevention of brain cell death. We would like to invite you to submit original research papers or review articles to this Special Issue on “Bioactive Compounds for Brain Ischemia and Neurodegenerative Disease”, addressing any research topic highlighting the recent identification of synthetic as well as natural-based bioactive molecules that alleviate brain cell damage.

Prof. Dr. Ramunė Morkūnienė
Dr. Dalia M. Kopustinskiene
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. Molecules 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.

Keywords

  • brain
  • neuroprotection
  • neurodegenerative diseases
  • ischemia
  • mitochondria
  • oxidative stress
  • inflammation
  • bioactive compounds

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

13 pages, 767 KiB  
Article
Inhibition of Enzymes Involved in Neurodegenerative Disorders and Aβ1–40 Aggregation by Citrus limon Peel Polyphenol Extract
by Rosaria Arcone, Antonio D’Errico, Rosarita Nasso, Rosario Rullo, Annarita Poli, Paola Di Donato and Mariorosario Masullo
Molecules 2023, 28(17), 6332; https://doi.org/10.3390/molecules28176332 - 30 Aug 2023
Cited by 1 | Viewed by 1193
Abstract
Alzheimer’s (AD) and Parkinson’s diseases (PD) are multifactorial neurogenerative disorders of the Central Nervous System causing severe cognitive and motor deficits in elderly people. Because treatment of AD and PD by synthetic drugs alleviates the symptoms often inducing side effects, many studies have [...] Read more.
Alzheimer’s (AD) and Parkinson’s diseases (PD) are multifactorial neurogenerative disorders of the Central Nervous System causing severe cognitive and motor deficits in elderly people. Because treatment of AD and PD by synthetic drugs alleviates the symptoms often inducing side effects, many studies have aimed to find neuroprotective properties of diet polyphenols, compounds known to act on different cell signaling pathways. In this article, we analyzed the effect of polyphenols obtained from the agro-food industry waste of Citrus limon peel (LPE) on key enzymes of cholinergic and aminergic neurotransmission, such as butyryl cholinesterase (BuChE) and monoamine oxidases (MAO)-A/B, on Aβ1–40 aggregation and on superoxide dismutase (SOD) 1/2 that affect oxidative stress. In our in vitro assays, LPE acts as an enzyme inhibitor on BuChE (IC50 ~ 73 µM), MAO-A/B (IC50 ~ 80 µM), SOD 1/2 (IC50 ~ 10–20 µM) and interferes with Aβ1–40 peptide aggregation (IC50 ~ 170 µM). These results demonstrate that LPE behaves as a multitargeting agent against key factors of AD and PD by inhibiting to various extents BuChE, MAOs, and SODs and reducing Aβ-fibril aggregation. Therefore, LPE is a promising candidate for the prevention and management of AD and PD symptoms in combination with pharmacological therapies. Full article
Show Figures

Graphical abstract

Back to TopTop