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 invention relates to an isolated truncated form of the secretory aspartyl proteinase 2, as well as to nucleic acid molecules encoding same. The present invention also relates to a composition comprising an isolated truncated form of the secretory aspartyl proteinase 2, as well as to nucleic acid molecules encoding same.

Inhibitors are provided for targeting -secretase to reduce amyloid load as a viable strategy in Alzheimer's disease treatment and drug discovery. -secretase has been shown to cleave amyloid precursor protein, causing an increase in extracellular concentration of amyloid- 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 -secretase to cleave the amyloid precursor protein, halting the build-up of extracellular amyloid- peptides. The inhibitors exhibit specificity for amyloid precursor proteins, reducing concerns of potential off-target effects.

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

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).

The present invention generally relates to aspartic proteases (EC 3.4.23) for producing cheese.

It relates to immune cells (e.g., T cells such as CAR-T cells, NK cells such as CAR-NK cells) modified to have no or reduced expression and/or function of one or more target proteins selected from the group consisting of: Signal Peptide Peptidase Like 3 (SPPL3), FADD, FAS, CASP8, ARID1A, BAK1, BID, ETS1, IKZF2, and HIST1H1B (such as SPPL3), uses thereof, and methods for generating thereof. Also provided are uses of the one or more target proteins (e.g., SPPL3) as a biomarker.