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).
At a recent meeting on “Research priorities for preventing and treating Alzheimer’s disease and related dementias” (ADRD), convened by the National Academies, one consensus priority on ADRD research was that there needs to be more of it at every stage. Several speakers presented stark numbers on the relative volume of research in cancer and neurodegeneration. Research output, measured in peer-reviewed papers, for dementia is estimated to be around 10,000 papers annually, compared to 150,000 for cancer, while AD clinical trials are also few and far between compared to cancer trials. This final installment of BioWorld’s series on Alzheimer’s explores some of the reasons for this discrepancy along with the latest advances and ongoing efforts to accelerate research and drug development in the field.
By independently manipulating the lifespan of worms and one of its purported biomarkers, namely, the cessation of vigorous movement (CVM), investigators at the Center for Genomic Regulation (CRG) in Barcelona have demonstrated that the two are driven by partly independent processes.
Tumor mutational burden (TMB), a biomarker used to assess whether a patient will respond to immunotherapy, needs to be recalculated in order to be useful for patients of Asian or African descent. Scientists at the Dana-Farber Cancer Institute found a significant bias in the estimated TMB values affecting these populations and adjusted them for those patients.