Targeting Protein Misfolding: From Alzheimer's Amyloids to Therapeutic Peptides
A special issue of Biomolecules (ISSN 2218-273X).
Deadline for manuscript submissions: 16 February 2026 | Viewed by 43
Special Issue Editor
Interests: Alzheimer’s disease; prion diseases; amyloidogenesis; inhibitors of amyloidogenesis; amyloid fibrils
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Protein misfolding accompanies many complex diseases, including Alzheimer’s disease, diabetes and prion diseases. Whether this process is at the center of the etiology of these diseases still remains an open question. Recently, the FDA approved monoclonal antibodies for use against β-amyloid species, showing a very moderate influence on the slowing of the course of Alzheimer’s disease. This observation suggests a multi-factorial etiology of this disease—where protein misfolding along with other processes contributes to neurodegeneration. Therefore, amyloidogenic events are still worth studying.
The mechanism of the misfolding of proteins into amyloids has been thoroughly studied. On the other hand, the dissolution of mature fibrils and neurotoxic oligomers has been studied much less. Monoclonal antibody therapy is very costly and unlikely to solve the problem of dementia and Alzheimer’s disease. For this Special Issue, in the quest for alternative solutions, supporting multi-factorial therapy, we welcome contributions dealing with the process of the dissolution of amyloid species, especially concerning β-amyloid, and those focusing on peptides called β-sheet breakers. Contributions on further topics are welcome. Both theoretical and experimental approaches as well as reviews are welcome.
Dr. Dariusz Stępkowski
Guest Editor
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Keywords
- amyloidogenesis
- amyloidosis
- amyloid fibrils
- dissolution of amyloid fibrils
- beta-sheet breakers
- peptide inhibitors
- small molecule inhibitors
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