The present invention relates to reconstituted high density lipoprotein (rHDL) formulations comprising an apolipoprotein, a lipid and a lyophilization stabilizer. Said formulations have reduced renal toxicity and good long-term stability, especially in lyophilized form.

This disclosure provides anti-apolipoprotein L1 (APOL1) antibodies, including anti-APOL1 antibodies that distinguish the GO and G1 forms from the G2 form of APOL1, distinguish APOL1 found on podocytes from that found on HDL particles in serum, and distinguish APOL1 from apolipoproteins L2, L3, L4 and L6 (APOL2, APOL3, APOL4 and APOL6), and methods of using the same.

A method for cultivating a bacterial cell comprising the addition of an amino acid in an alkaline solution used for pH regulation. Also an aspect is a method for producing a polypeptide comprising the steps of a) providing a bacterial cell comprising a nucleic acid encoding the polypeptide, b) cultivating the provided cell, c) adjusting the pH value during the cultivating with a basic solution comprising an amino acid, d) recovering the polypeptide from the cell or the cultivation medium and thereby producing the polypeptide.

A method for cultivating a bacterial cell comprising the addition of an amino acid in an alkaline solution used for pH regulation. Also an aspect is a method for producing a polypeptide comprising the steps of a) providing a bacterial cell comprising a nucleic acid encoding the polypeptide, b) cultivating the provided cell, c) adjusting the pH value during the cultivating with a basic solution comprising an amino acid, d) recovering the polypeptide from the cell or the cultivation medium and thereby producing the polypeptide.

A non-human transgenic animal expressing ApoL1 is provided as well as a method for generating the same. Also provided is a method for identifying an agent capable of reducing the progression of an ApoL1 mediated nephropathy. Furthermore, an isolated antibody is provided which binds to the human variants of ApoL1.

The present disclosure relates to lipoprotein complexes and lipoprotein populations and their use in the treatment and/or prevention of dyslipidemic diseases, disorders, and/or conditions. The disclosure further relates to recombinant expression of apolipoproteins, purification of apolipoproteins, and production of lipoprotein complexes using thermal cycling-based methods.

The present disclosure relates to lipoprotein complexes and lipoprotein populations and their use in the treatment and/or prevention of dyslipidemic diseases, disorders, and/or conditions. The disclosure further relates to recombinant expression of apolipoproteins, purification of apolipoproteins, and production of lipoprotein complexes using thermal cycling-based methods.

The present disclosure provides methods of determining A-beta in a mammal before and after treatment of an amyloid disorder, comprising obtaining a first blood sample from the mammal; administering to the mammal a treatment for an amyloid disorder; obtaining a second blood sample from the mammal; quantifying a level of A-beta in the first blood sample and in the second blood sample; and determining the level of A-beta in the mammal before and after treatment of the amyloid disorder.

Methods for treating neurologic diseases, e.g., amyotrophic lateral sclerosis (ALS) and multiple sclerosis, by modulating the APOE-TGFbeta pathway. The methods include administering one or more inhibitory nucleic acids targeting Trem2 and/or ApoE), sense nucleic acids encoding Egr1 and/or Mertk, and/or antibodies that bind to and inhibit Trem2 and/or ApoE.

Disclosed are yeast cells expressing a polypeptide comprising a signal sequence and a human ApoE protein. In some embodiments the polypeptide comprises ApoE2. In some embodiments the polypeptide comprises ApoE3. In some embodiments the polypeptide comprises ApoE4. Also disclosed are methods of screening yeast cells to identify compounds that prevent or suppress Apo-induced toxicity. Compounds identified by such screens can be used to treat or prevent neurodegenerative disorders such as Alzheimer's disease. Also disclosed are methods of screening yeast cells to identify genetic suppressors or enhancers of ApoE-induced toxicity. Also disclosed are genetic suppressors or enhancers of ApoE-induced toxicity identified using the methods, and human homologs thereof. Also disclosed are methods of identifying compounds that modulate expression or activity of genetic modifiers of ApoE-induced toxicity.