Recent Advances in Understanding and Treating Amyloidosis

Dear Colleagues,

Amyloidosis is a hallmark of several neurodegenerative disorders (NDs) that afflict large numbers of the world's population. To date, approximately 50 distinct human pathologies, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), have been related to the accumulation of amyloid deposits that consist of ordered protein assemblies formed by a specific peptide or protein. Several factors appear to affect the fate of the amyloid proteins, including metal transition ions and oxidative stress.

Amyloid-β, α-synuclein, and transactive response DNA-binding protein 43 (TDP43), which are involved in AD, PD, and ALS, possess metal-binding sites that have been linked to their neurotoxicity. The binding with metal ions triggers the formation of toxic oligomers and aggregates but, often, also the production of reactive oxygen species.

Despite numerous efforts to advance our understanding of ND etiology and constant research on effective therapies, our information remains incomplete because many potential mechanisms are implicated in neurodegeneration. This Special Issue aims to highlight recent advances in our understanding of the toxic mechanisms involved in NDs and new therapeutic opportunities to modulate self- and metal-induced amyloid aggregation and toxicity.

We welcome original research papers, review articles, and short communications on recent advances and emerging concepts in amyloid-related research.

Dr. Valentina Oliveri
Guest Editor