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Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches

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Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are characterized by the progressive degeneration of the nervous system. These diseases result in the progressive and irreversible loss of neurons, leading to cognitive decline or motor dysfunction. The best-known neurodegenerative diseases are Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Neurodegeneration can result from different mechanisms: (a) Protein misfolding and aggregation. Beta-amyloid peptide and tau protein have been implicated in Alzheimer's disease, alpha-synuclein in Parkinson's disease, and huntingtin in Huntington’s disease. (b) Oxidative stress damages cellular structures, including neurons, and may contribute to their degeneration. (c) Chronic inflammation within the nervous system can exacerbate neuronal damage and contribute to the progression of neurodegenerative diseases. (d) Mutations in specific genes can increase an individual’s susceptibility to developing these diseases. For example, mutations in the APP, PSEN1, and PSEN2 genes are associated with familial forms of early onset Alzheimer's disease.

The aim of this Special Issue of Biomedecines is to present mechanisms involved in neurodegenerative diseases, or to outline therapeutic approaches with their progress and pitfalls.

Dr. Marie-Lise Maddelein
Guest Editor

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Keywords

neurodegenerative diseases
neurons
mechanism

Published Papers (2 papers)

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Research

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18 pages, 3245 KiB

Open AccessArticle

Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations

by Khalid Saad Alharbi

Biomedicines 2024, 12(3), 625; https://doi.org/10.3390/biomedicines12030625 - 12 Mar 2024

Viewed by 876

Abstract

Huntington’s disease (HD) is a neurodegenerative disease that causes progressive motor and cognitive dysfunction. There is no cure for HD, and current therapeutics can only manage the signs and symptoms as well as slowing disease progression. This investigation examines the possible therapeutic advantages of europinidin in 3-nitropropionic acid (3-NPA) injected HD in rats. Wistar rats were randomly assigned to five groups (n = 6): normal control, 3-NPA (10 mg/kg, i.p.), 3-NPA + europinidin-10 (10 mg/kg, p.o.), 3-NPA + europinidin-20 (20 mg/kg, p.o.), and europinidin alone (20 mg/kg, p.o.) for 15-day. Various behavioral and biochemical parameters including antioxidant levels, oxidative stress, pro-inflammatory markers, mitochondrial enzyme complex, and neurotransmitters were assessed. Europinidin restored biochemical, mitochondrial dysfunction, oxidative stress, neurotransmitter, and pro-inflammatory parameters disrupted by 3-NPA. Here we show that europinidin attenuates 3-NPA-induced neurodegeneration in rat models of HD. Europinidin modulates oxidative stress, enhances antioxidants, restores mitochondrial enzyme complex activity, reduces neuroinflammation, and modulates neurotransmitter levels. Our findings reveal the potential of europinidin as a novel therapeutic agent for the treatment of HD. This study also provides new insights into the molecular mechanisms of europinidin-mediated neuroprotection and may have a beneficial role in the management of neurological diseases. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches)

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Review

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14 pages, 1193 KiB

Open AccessReview

Passive Anti-Amyloid Beta Immunotherapies in Alzheimer’s Disease: From Mechanisms to Therapeutic Impact

by Thomas Gabriel Schreiner, Cristina Georgiana Croitoru, Diana Nicoleta Hodorog and Dan Iulian Cuciureanu

Biomedicines 2024, 12(5), 1096; https://doi.org/10.3390/biomedicines12051096 - 15 May 2024

Viewed by 625

Abstract

Alzheimer’s disease, the most common type of dementia worldwide, lacks effective disease-modifying therapies despite significant research efforts. Passive anti-amyloid immunotherapies represent a promising avenue for Alzheimer’s disease treatment by targeting the amyloid-beta peptide, a key pathological hallmark of the disease. This approach utilizes monoclonal antibodies designed to specifically bind amyloid beta, facilitating its clearance from the brain. This review offers an original and critical analysis of anti-amyloid immunotherapies by exploring several aspects. Firstly, the mechanisms of action of these therapies are reviewed, focusing on their ability to promote Aβ degradation and enhance its efflux from the central nervous system. Subsequently, the extensive history of clinical trials involving anti-amyloid antibodies is presented, from initial efforts using first-generation molecules leading to mixed results to recent clinically approved drugs. Along with undeniable progress, the authors also highlight the pitfalls of this approach to offer a balanced perspective on this topic. Finally, based on its potential and limitations, the future directions of this promising therapeutic strategy for Alzheimer’s disease are emphasized. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: From Mechanisms to Therapeutic Approaches)

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