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Dear Colleagues,

Neurodegenerative diseases, including Alzheimer’s, Parkinson’s, and others, are age-related multifactorial pathologies, in which complex events lead to impairment of brain activity with cognitive disability as the main clinical hallmark. Amyloid cascade and neuroinflammation are their most obvious and closely interlinked pathological manifestations. The underlying cause of the amyloid cascade is the failure of specific peptides/proteins to adopt and retain their native structure, leading to self-assembly into amyloid oligomers and fibrils and growing amyloid burden. The amyloid conversion results in the loss of physiological function and gain of amyloid cytotoxicity. The latter is linked to derangement of both specific signalling pathways and several homeostatic cell functions. Basic science and clinical research have made extraordinary progress in the last two decades, providing insights into the mechanisms of pathological aggregation and in discovering new diagnostic tools and therapeutic options. Due to the biological complexity of diseases, the multidisciplinary approach may bridge the gap between experimental models and disease in patients. In this issue, the research linking in vitro, in vivo, and ex vivo studies are welcome to address this very complex and challenging problem, and shed light on the triggers, causes, mechanisms, and treatment of neurodegenerative diseases. We may not solve all problems but “wisdom begins in wonders” (Socrates).

Prof. Dr. Ludmilla A. Morozova-Roche
Dr. Igor A. Iashchishyn
Guest Editors

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Keywords

neurodegenerative disease
Alzheimer’s
Parkinson’s
amyloid
neuroinflammation
models
amyloid mechanisms
cytotoxicity
disease prevention
disease cause

Published Papers (2 papers)

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Research

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16 pages, 3006 KiB

Open AccessArticle

Hypoxic and Hypercapnic Responses in Transgenic Murine Model of Alzheimer’s Disease Overexpressing Human AβPP: The Effects of Pretreatment with Memantine and Rivastigmine

by Kryspin Andrzejewski, Monika Jampolska, Ilona Mojzych, Silvia V. Conde and Katarzyna Kaczyńska

Int. J. Mol. Sci. 2022, 23(11), 6004; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23116004 - 26 May 2022

Cited by 2 | Viewed by 1488

Abstract

Despite the severe respiratory problems reducing the quality of life for Alzheimer’s disease (AD) patients, their causes are poorly understood. We aimed to investigate hypoxic and hypercapnic respiratory responses in a transgenic mouse model of AD (AβPP V717I) overexpressing AβPP and mimicking early-onset AD. The cholinesterase inhibitor rivastigmine and the NMDA receptor antagonist memantine were used to investigate the effects of drugs, used to treat AD cognitive dysfunction, on breathing in hypoxia and hypercapnia. We found a significant increase in the respiratory response to hypercapnia and no difference in the hypoxic response in APP+ mice, compared with the control group (APP−). Memantine had no effect on respiration in either group, including responses to hypoxia and hypercapnia. Rivastigmine depressed resting ventilation and response to hypercapnia irrespective of the mice genotype. Reduction in hypoxia-augmented ventilation by rivastigmine was observed only in APP+ mice, which exhibited lower acetylcholinesterase activity in the hippocampus. Treatment with rivastigmine reduced the enzyme activity in both groups equally in the hippocampus and brainstem. The increased ventilatory response to hypercapnia in transgenic mice may indicate alterations in chemoreceptive respiratory nuclei, resulting in increased CO₂ sensitivity. Rivastigmine is a potent reductant of normoxic and hypercapnic respiration in APP+ and APP− mice. Full article

(This article belongs to the Special Issue Connecting In Vitro, In Vivo, and Ex Vivo Studies in Neurodegenerative Diseases)

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Review

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37 pages, 1939 KiB

Open AccessReview

Deconstructing Alzheimer’s Disease: How to Bridge the Gap between Experimental Models and the Human Pathology?

by Anaïs Vignon, Lucie Salvador-Prince, Sylvain Lehmann, Véronique Perrier and Joan Torrent

Int. J. Mol. Sci. 2021, 22(16), 8769; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168769 - 16 Aug 2021

Cited by 13 | Viewed by 5062

Abstract

Discovered more than a century ago, Alzheimer’s disease (AD) is not only still present in our societies but has also become the most common dementia, with 50 million people worldwide affected by the disease. This number is expected to double in the next generation, and no cure is currently available to slow down or stop the disease progression. Recently, some advances were made due to the approval of the aducanumab treatment by the American Food and Drug Administration. The etiology of this human-specific disease remains poorly understood, and the mechanisms of its development have not been completely clarified. Several hypotheses concerning the molecular mechanisms of AD have been proposed, but the existing studies focus primarily on the two main markers of the disease: the amyloid β peptides, whose aggregation in the brain generates amyloid plaques, and the abnormally phosphorylated tau proteins, which are responsible for neurofibrillary tangles. These protein aggregates induce neuroinflammation and neurodegeneration, which, in turn, lead to cognitive and behavioral deficits. The challenge is, therefore, to create models that best reproduce this pathology. This review aims at gathering the different existing AD models developed in vitro, in cellulo, and in vivo. Many models have already been set up, but it is necessary to identify the most relevant ones for our investigations. The purpose of the review is to help researchers to identify the most pertinent disease models, from the most often used to the most recently generated and from simple to complex, explaining their specificities and giving concrete examples. Full article

(This article belongs to the Special Issue Connecting In Vitro, In Vivo, and Ex Vivo Studies in Neurodegenerative Diseases)

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