Mutations are at the root of many human diseases. Still, we largely do not exactly
understand how they trigger pathogenesis. One, more recent, hypothesis has been that they …

Protein therapeutics carry inherent limitations of membrane impermeability and structural
instability, despite their predominant role in the modern pharmaceutical market. Effective …

Expression of many disease-related aggregation-prone proteins results in cytotoxicity and
the formation of large intracellular inclusion bodies. To gain insight into the role of inclusions …

Huntington's disease is a neurodegenerative disorder caused by a CAG expansion in the
first exon of the HTT gene, resulting in an extended polyglutamine (poly-Q) tract in huntingtin …

A long-standing goal of amyloid research has been to characterize the structural basis of the
rate-determining nucleating event. However, the ephemeral nature of nucleation has made …

Neurodegeneration in Huntington's disease (HD) is accompanied by the aggregation of
fragments of the mutant huntingtin protein, a biomarker of disease progression. A particular …

Amyloid-β (Aβ) fibrils in neuritic plaques are a hallmark of Alzheimer's disease (AD). Since
the 42-residue Aβ (Aβ42) fibril is the most pathogenic among different Aβ species, its …

Solid-state nuclear magnetic resonance (ssNMR) spectroscopy enables the structural
characterization of a diverse array of biological assemblies that include amyloid fibrils, non …

The lack of detailed insight into the structure of aggregates formed by the huntingtin protein
(HTT) has hampered the efforts to develop therapeutics and diagnostics targeting pathology …

Huntington's disease is a progressive neurodegenerative disease caused by expansion of
the polyglutamine domain in the first exon of huntingtin (HttEx1). The extent of expansion …