Co-aggregation, amyloid formation, and unidirectional cross-seeding of prolactin and galanin for their efficient storage in secretory granules of pituitary and subsequent functional hormone release.

Inter-molecular cross-seeding between phenol-soluble modulins facilitates rapid and efficient self-assembly in Staphylococcus aureus biofilms revealing a complex molecular interplay between distinct phenol-soluble modulins orchestrating functional amyloid formation.

The amyloid patterns overlap with the default-mode network, whereas the tau patterns overlap with distinct functional networks and are associated with a loss of anatomical connectivity and multiple cognitive functions.

Age-dependent protein aggregation closely resembles protein aggregation associated with neurodegenerative diseases and other amyloidoses, and initiates early functional decline in different tissues.

Ex vivo characterization of the interaction of human sperm with semen factors reveals that semen amyloids, previously discovered due to their ability to enhance HIV infection, serve a physiological function by promoting disposal of the defective sperm.

Tau deposition in the aging brain follows patterns of functional connectivity that correspond to specific neural memory networks, and this relationship is strengthened in the presence of amyloid-β.

The role of amyloid-β-aggregation sequence and of the various domains in the physiological function of the FLO11-encoded adhesin in the yeast Saccharomyces cerevisiae are disclosed in this report.

Production of an amyloid protein by bacteria within the gut microbiome can influence the pathophysiology of a mouse model of synucleinopathy.

Machine learning-based models of brain age using distinct MRI modalities (structural MRI and functional connectivity) capture complementary signals related to healthy age differences and capture unique patterns related to Alzheimer disease, including stages of disease progression, biomarkers, and cognition.

Cognitively normal older adults show a positive relationship between neural activity during memory encoding and brain β-amyloid deposition rate over the subsequent 3-4 years, supporting preclinical data that associates neural activity with β-amyloid deposition.