A method of treating Alzheimer's Disease (AD) is disclosed. The method comprises administering to the subject a therapeutically effective amount of an agent which prevents the binding of amyloid precursor protein (APP) to Tau protein.

The present invention is directed to a pharmaceutical composition comprising Cannabidiol and a method of use thereof, i.e., for treating or preventing bronchiolitis obliterans in a subject.

A method for treatment of a subject having an inflammatory disease of the epithelium comprising the step of administering an amount of a composition comprising an isolated bacterial amyloid peptide to said subject. In embodiments, the composition is membrane-free. In embodiments, the composition comprises a curli fibril. In yet further embodiments, the isolated bacterial amyloid peptide is a CsgA polypeptide, a CsgA polypeptide fragment, a CsgB polypeptide or a CsgB polypeptide fragment. Also provided is a method for decreasing epithelium permeability in a tissue of a subject comprising epithelium comprising the step of administering an amount of a composition comprising an isolated bacterial amyloid peptide to the epithelium of the subject. In embodiments, the composition is membrane-free. In further embodiments, the composition comprises a curli fibril. In embodiments, the isolated bacterial amyloid peptide is a CsgA polypeptide, a CsgA polypeptide fragment, a CsgB polypeptide or a CsgB polypeptide fragment.

The present invention relates to a chimeric protein comprising at least one human amyloid P component and at least one fragment of an Fc region of a human antibody, the human amyloid P component and the fragment of an Fc region with which it is associated being bound to each other by means of a hinge region.

The present invention relates to SAP-Fc fusion proteins and methods of treating amyloid related diseases.

The invention relates to polypeptides that comprise a portion of filamentous bacteriophage gene 3 protein (g3p) sufficient to bind to and/or disaggregate amyloid, e.g., the N1-N2 portion of g3p and mutants and fragments thereof, wherein that g3p amino acid sequence has been modified through amino acid deletion, insertion or substitution to remove a putative glycosylation signal. The invention further relates to such polypeptides that are also modified through additional amino acid substitution to be substantially less immunogenic than the corresponding wild-type g3p amino acid sequence when used in vivo. The polypeptides of the invention retain their ability to bind and/or disaggregate amyloid. The invention further relates to the use of these g3p-modified polypeptides in the treatment and/or prevention of diseases associated with misfolding or aggregation of amyloid.

Apparatuses and methods are provided. Some methods may include providing a substrate to a processing chamber, the substrate having a first material adjacent to and covering a surface of a second material, modifying a layer of the first material by flowing a first process gas onto the substrate and thereby creating a modified layer of the first material, removing the modified layer of the first material by flowing a second process gas onto the substrate, and converting, when the surface of the second material is uncovered via removal of the modified layer, the surface to a converted layer of the second material by flowing a third process gas onto the substrate, in which the first and second process gases are less reactive with the converted layer than with the first material and the second material.

Tau protein misfolding, aggregation and accumulation in the nervous system is an abnormal event which is responsible for widespread synaptic loss and neurodegeneration; it can occur spontaneously or can be triggered by misfolding of amyloid β protein. The present invention concerns the use of hexapeptide Aβ1-6.sub.A2V(D) in the treatment of a family of neurodegenerative diseases related to tau pathology. In the present studies, Aβ1-6.sub.A2V(D) is shown capable of interfering with protein tau at different levels. This property, in association with additional neuroprotective activities of Aβ1-6.sub.A2V(D), offers as a whole an excellent therapeutic asset against tau protein-related diseases. Moreover, the intranasal administration of Aβ1-6.sub.A2V(D) obtains remarkable levels of permeation of this peptide through the blood-brain barrier, with widespread distribution thereof among the most important brain areas involved in tau pathology.

The present invention relates to the treatment of Alzheimer's disease. Provided is the use of an reagent for regulating the relative abundance of intestinal microorganisms in the preparation of a medicament for treating Alzheimer's disease in a subjet.

Antibody for human amyloid beta. Antibody selectively binds human amyloid beta 42 peptide over human amyloid beta 40 peptide. Antibodies specific for amyloid beta 42 as therapeutic agents for binding amyloid beta 42 peptide and treating conditions associated with amyloidosis, such as Alzheimer's disease.