Alzheon Inc. has raised $100 million in a series E financing round to push its oral drug candidate for early Alzheimer’s disease (AD), ALZ-801 (valiltramiprosate), through a late-stage, Apolloe4 study.
Based on its analysis of a large cohort of individuals homozygous for the ε4 variant of apolipoprotein E (APOE4), a multinational team of researchers is arguing that homozygosity for APOE4 should be considered a genetic form of Alzheimer’s disease. However, not everyone agrees that the findings warrant reclassifying APOE from risk factor to causal gene. Currently, APOE4 is classified as the strongest risk factor for developing AD. Another variant, the APOE2 variant, is protective, while APOE3 is neutral.
Based on its analysis of a large cohort of individuals homozygous for the ε4 variant of apolipoprotein E (ApoE4), a multinational team of researchers is arguing that homozygosity for ApoE4 should be considered a genetic form of Alzheimer’s disease (AD).
The shunt towards, or away from, cognitive decline may happen decades before such decline becomes clinically evident. And known risk factors explain very little of that decline. That is the conclusion reached by researchers from the Ohio State University, who published their results in the Feb. 8, 2023, issue of PLOS ONE.
In their analysis, the team looked at both the absolute level of cognitive function in about 7,000 participants of the U.S. Health and Retirement Study at age 54, and at the decline in cognitive function from age 54 to 85. The study participants that were analyzed were born between 1931 and 1941. The results were reminiscent of the adage that the way to make a silk purse out a sow’s ear is to start with a silk sow.
Carrying the apolipoprotein E4 allele (APOE4), and not the APOE3 variant, is the strongest risk factor for developing Alzheimer’s disease (AD). But the underlying mechanism has remained elusive. Now, researchers at MIT and Mount Sinai have found that in brains carrying the APOE4 allele, lipid and cholesterol processes were dysregulated in oligodendrocytes and that this effect reduced myelination.
A study led by scientists at the University of Science and Technology of China in Hefei City is the first to show that astrocytic apolipoprotein E (ApoE) regulates neuronal epigenetic states via reprogramming lipid metabolism, which was shown to control brain function, in particular memory consolidation, in mice.
Variants in the APOE gene are the strongest genetic risk factor for developing Alzheimer’s disease (AD). Now, researchers at Rockefeller University have demonstrated that APOE variants also affected the risk of progression and metastasis as well as the response to immunotherapy, in melanoma.
Variants in the APOE gene are the strongest genetic risk factor for developing Alzheimer’s disease (AD). Now, researchers at Rockefeller University have demonstrated that APOE variants also affected the risk of progression and metastasis as well as the response to immunotherapy, in melanoma.
