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Neurological Diseases: From Physiology to Therapy

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: 20 October 2025 | Viewed by 1251

Special Issue Editor


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Guest Editor
Physiology, Department of Biomedical Sciences, School of Health Sciences, International Hellenic University, 57400 Thessaloniki, Greece
Interests: Alzheimer's disease; mild cognitive impairment; cerebrospinal fluid; beta amyloid; neurodegenerative diseases; neurodegeneration; cognition disorders; event-related potentials; evoked potentials
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Special Issue Information

Dear Colleagues,

The diagnosis of neurological diseases is one of the most difficult challenges for medical professionals due to the complexity of the nervous system. Currently, more than 600 diseases have been identified including neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, cerebrovascular diseases, and others such as multiple sclerosis, migraine, neuroinfections, and neuromuscular diseases. According to a World Health Organization report, nervous system diseases affect up to one billion people worldwide. Neurological diseases include those caused by single gene abnormalities, such as Huntington’s disease, spinocerebellar degeneration, and muscular dystrophy, and multifactorial diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS).

In this Special Issue of “Neurological Diseases: From Physiology to Therapy”, we invite investigators to contribute original research, review articles, or case reports focusing on the research area that extends from physiology and genetics to the treatment of neurological diseases.

Dr. Vasileios Papaliagkas
Guest Editor

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Keywords

  • neurophysiology
  • genetics
  • Alzheimer’s disease
  • neurological diseases
  • neurodegenerative diseases

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Published Papers (1 paper)

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9 pages, 561 KB  
Opinion
Anti-Amyloid Therapies for Alzheimer’s Disease: Progress, Pitfalls, and the Path Ahead
by Vasileios Papaliagkas
Int. J. Mol. Sci. 2025, 26(19), 9529; https://doi.org/10.3390/ijms26199529 - 29 Sep 2025
Viewed by 1103
Abstract
Anti-amyloid monoclonal antibodies have finally achieved their translational breakthrough after many years of unmet expectations. The FDA granted traditional approval to lecanemab in July 2023, and the European Medicines Agency approved it in late 2024 with specific genetic restrictions; meanwhile, donanemab received FDA [...] Read more.
Anti-amyloid monoclonal antibodies have finally achieved their translational breakthrough after many years of unmet expectations. The FDA granted traditional approval to lecanemab in July 2023, and the European Medicines Agency approved it in late 2024 with specific genetic restrictions; meanwhile, donanemab received FDA approval in July 2024 and EMA marketing authorization just one month ago. These agents consistently clear cerebral amyloid and slow clinical decline modestly in early-stage, biomarker-confirmed Alzheimer’s disease (AD). On the other hand, they also create significant safety risks, including amyloid-related imaging abnormalities (ARIA) and substantial operational requirements for health systems that are already under pressure. Therefore, precise risk management based on APOE genotyping and the presence of cerebral amyloid angiopathy and cerebral microbleeds should be performed before therapy is initiated. The near-term agenda should prioritize the following areas of study: (1) biomarker-driven front-end triage (including emerging plasma assays); (2) ARIA-aware care pathways and shared decision making; (3) outcome-based coverage and rational pricing; (4) clinical trials that layer anti-amyloid therapy into combinatorial strategies targeting tau protein, neuroinflammation, and synaptic resilience. Full article
(This article belongs to the Special Issue Neurological Diseases: From Physiology to Therapy)
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