This invention relates to inhibitory peptides which bind to α-synuclein molecules and inhibit α-synuclein amyloidogenic aggregation, α-synuclein cytotoxicity, and spread of α-synuclein. Methods of making and using the inhibitory peptides (e.g. to treat subjects having conditions or diseases that are mediated by α-synuclein, such as Parkinson's disease, dementia with Lewy bodies, or MSA) are described.

Methods of making engineered protein-based materials, nanofibers, and biofilms from bacterial amyloid-based structures that are capable of mediating long-range electron transport are provided.

This invention relates to the field of tau aggregation inhibitors. More specifically, the invention relates to anti-amyloid therapeutics. More specifically, the invention provides pharmaceutical compositions and methods of treating aggregation associated conditions or diseases with certain peptides.

The present invention relates to CD271-interacting peptides and derivatives thereof and to their use as a medicament for the treatment of CD271-related diseases, in particular for the treatment of melanoma and other CD271-related skin diseases.

The current Alzheimer's disease model mouse, developed by manipulating the expression of a gene directly related to distinctive pathology that is specific to the disease, such as acceleration of amyloid plaque deposition, is a model of a preclinical state, or of a pathology that is fundamentally different from human Alzheimer's disease. In view of the current state described above, the present invention addresses the problem of developing a non-human transgenic animal in which Alzheimer's pathology is more accurately reflected, and thereby elucidating a disease mechanism or contributing to drug discovery. In the present invention, by heterozygous knockout of the drebrin gene of a non-human Alzheimer's disease model animal used as a base, senescence risk can be imparted to the conventional non-human Alzheimer's disease model animal. Alzheimer's pathology is more accurately reflected in this non-human Alzheimer's disease model animal.

A novel constrained peptide epitope derived from Aβ, related antibody compositions and methods of use. An isolated antibody that specifically binds to a cyclic peptide comprising the conformational epitope corresponding to a solvent-exposed, antibody accessible knuckle region of oligomeric Aβ is described. An antigenic peptide comprising an epitope having a constrained cyclic configuration, corresponding to a solvent-exposed, antibody accessible knuckle region of oligomeric Aβ is also described. Methods of treating, preventing, and diagnosing Alzheimer's disease are also described.

The invention relates to isolated recombinant peptides comprising an epitope from human tau 2N4R. The invention also relates to use of such peptides to generate binding molecules, such as antibodies, specific for the tau epitope and to such peptides and antibodies for use in investigation, diagnosis and treatment of tauopathies, such as Alzheimer’s disease.

The present invention relates to methods of treating neurodegenerative disorders associated with Alzheimer's disease (AD), Parkinson's disease (PD) and synucleinopathies, such as dementia with Lewy bodies, Down Syndrome (DS) and associated cognitive disorders, multiple system atrophy, and rare neuroaxonal dystrophies, such as Niemann-Pick type C disease (NPC) and Gaucher's disease comprising administering an inhibitor to disrupt the interaction between Aβ or αS and neuronal lipids. The invention further relates to assays for identifying agents that reduce interaction between Aβ or αS and neuronal lipids. Lastly, the invention relates to methods and compositions for intranasal administration of fatty acids or lipids containing fatty acid acyl chains of dietary lipids for promoting central nervous system health and/or prevention or treatment of neurodegenerative disorders.

Aspects of the present disclosure include amyloid β (Aβ) peptides. In certain aspects, the Aβ peptides include a chiral substitution at an electrostatic cluster amino acid residue. Also provided are compositions, non-human animals, and kits that include the Aβ peptides. Methods involving the Aβ peptides are also provided.

The present invention provides non-natural molecules which comprise a peptide part able to stop the amyloid aggregation which is fused to a moiety which stimulates the proteasomal degradation pathway in the cell. Non-natural molecules of the invention are useful to treat human and veterinary pathological aggregation disorders.