The present invention relates to the finding of methods to shift the glycosylation profile of recombinant produced serum glycoproteins to the predominant bi-antennary form found in human plasma. This is accomplished by providing a mammalian cell line according to the invention with a series of gene disruptions and/or gene insertions that facilitate this shift.

The present disclosure relates generally to detection of molecular biomarkers in a sample or diagnosis of a subject based upon detection or quantification of molecular biomarkers in a sample, specifically to the identification and use of biomarkers for pancreatic cysts.

Inhibitors are provided for targeting γ-secretase to reduce amyloid load as a viable strategy in Alzheimer's disease treatment and drug discovery. γ-secretase has been shown to cleave amyloid precursor protein, causing an increase in extracellular concentration of amyloid-β peptides. This extracellular concentration increase can lead to build-up amyloid plaques in patients and associated health complications for them. The inhibitors bind to a C-terminal lysine cluster adjacent the transmembrane domain of amyloid precursor protein through both covalent and non-covalent interactions. These interactions inhibit the ability of γ-secretase to cleave the amyloid precursor protein, halting the build-up of extracellular amyloid-β peptides. The inhibitors exhibit specificity for amyloid precursor proteins, reducing concerns of potential off-target effects.

The present invention relates to the finding of methods to shift the glycosylation profile of recombinant produced semm glycoproteins to the predominant bi-antennary form found in human plasma. This is accomplished by providing a mammalian cell line according to the invention with a series of gene disruptions and/or gene insertions that facilitate this shift.

Methods and compositions for the treatment or prevention of amyloidosis are provided. In some embodiments, the methods comprise administering to the subject a therapeutically effective amount of at least one catabolic enzyme or a biologically active fragment thereof. Such methods and compositions may be employed to reduce, prevent, degrade and/or eliminate amyloid formation in the lysosome and/or extracellularly.

The present disclosure provides, among other things, methods for using presenilin based gene therapy to treat neurodegenerative dementia including, but not limited to Alzheimers disease, frontotemporal dementia, frontotemporal lobar degeneration, Picks disease, Lewy body dementia, memory loss, and cognitive impairment including mild cognitive impairment (MCI).

A liquid or dried granulated milk clotting aspartic protease enzyme composition and process for isolating a milk clotting aspartic protease enzyme of interest.

The present invention relates to dual-site BACE1 inhibitors, their manufacture, pharmaceutical compositions containing them and their use as therapeutically active substances. The active compounds of the present invention are useful in the therapeutic and/or prophylactic treatment of e.g. Alzheimer's disease.

A liquid or dried granulated milk clotting aspartic protease enzyme composition and process for isolating a milk clotting aspartic protease enzyme of interest.

Described herein are methods, systems and compositions for the treatment of neurodegenerative diseases and disorders. In various embodiments neurotrophins, such as Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) can be used for the treatment methodologies contained herein. In one embodiment, a method of treatment of Alzheimer's Disease by administering a composition comprising PACAP.