The EMA has changed its mind about an earlier decision that the risks of Leqembi (lecanemab) outweigh the benefits and is now recommending the Alzheimer’s disease drug is approved for a subgroup of patients. That follows an appeal by Eisai Co. Ltd. and a re-examination of the data, after details relating to 274 patients with two copies of the ApoE4 gene were removed from the file.
Reducing microglial activity in the presence of apolipoprotein E4 (APOE4) has uncovered a mechanism associated with the deposition of misfolded amyloid and tau in a novel mouse model of Alzheimer’s disease. By transplanting human neurons into the mouse brain and eliminating the mouse microglia, scientists at the Gladstone Institutes in San Francisco observed that amyloid and tau deposition was reduced. These results support therapeutic strategies that target APOE4 and microglia.
The E4 variant of the APO gene, the R47H variant of the TREM2 gene, and female sex are three of the strongest risk factors for the development of Alzheimer’s disease (AD). By combining all three of them in a mouse model of tauopathy, researchers at Weill Cornell Medical School have identified microglial inflammation and senescence as processes that occurred more strongly in female mice as tauopathy developed.
Seoul, South Korea-based Adel Inc. raised ₩17 billion (US$12.39 million) in bridge financing to advance its pipeline of Alzheimer’s disease therapies, including its tau antibody-based ADEL-Y01 candidate, currently in a U.S.-based phase I study.
Seoul, South Korea-based Adel Inc. raised ₩17 billion (US$12.39 million) in bridge financing to advance its pipeline of Alzheimer’s disease therapies, including its tau antibody-based ADEL-Y01 candidate, currently in a U.S.-based phase I study.
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.
