APOE loss-of-function variants: Compatible with longevity and associated with resistance to Alzheimer's disease pathology.

The ε4 allele of apolipoprotein E (APOE) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD). Knockdown of ε4 may provide a therapeutic strategy for AD, but the effect of APOE loss of function (LoF) on AD pathogenesis is unknown. We searched for APOE LoF variants in a large cohort of controls and patients with AD and identified seven heterozygote carriers of APOE LoF variants.

APOE-ε4 and BIN1 increase risk of Alzheimer's disease pathology but not specifically of Lewy body pathology.

Lewy body (LB) pathology commonly occurs in individuals with Alzheimer's disease (AD) pathology. However, it remains unclear which genetic risk factors underlie AD pathology, LB pathology, or AD-LB co-pathology. Notably, whether APOE-ε4 affects risk of LB pathology independently from AD pathology is controversial.

loss-of-function variants: Compatible with longevity and associated with resistance to Alzheimer's Disease pathology.

The ε4 allele of apolipoprotein E () is the strongest genetic risk factor for sporadic Alzheimer's Disease (AD). Knockdown of this allele may provide a therapeutic strategy for AD, but the effect of loss-of-function (LoF) on AD pathogenesis is unknown. We searched for LoF variants in a large cohort of older controls and patients with AD and identified six heterozygote carriers of LoF variants.

- 4 and increase risk of Alzheimer's disease pathology but not specifically of Lewy body pathology.

Lewy body (LB) pathology commonly occurs in individuals with Alzheimer's disease (AD) pathology. However, it remains unclear which genetic risk factors underlie AD pathology, LB pathology, or AD-LB co-pathology. Notably, whether - 4 affects risk of LB pathology independently from AD pathology is controversial.

A 3'UTR Insertion Is a Candidate Causal Variant at the Locus Associated with Increased Risk for FTLD-TDP.

Background And Objectives: Single nucleotide variants near associate with risk of frontotemporal lobar dementia with TDP-43 inclusions (FTLD-TDP) and Alzheimer's disease (AD) in genome-wide association studies (GWAS), but the causal variant at this locus remains unclear. Here we asked whether a novel structural variant on is the causal variant.

Methods: An exploratory analysis identified structural variants on neurodegeneration-related genes.

F-18 Fluciclovine PET-CT Findings and Pseudoprogression on Immunotherapy.

Immunotherapy plays a vital role in the treatment of several types of malignancies. While the molecular targets of immunotherapy differ, the desired goal is to increase the host immune response against neoplastic tissue. This upregulated immune state results in infiltration of the tumor with activated immune cells and may be misinterpreted as disease progression in anatomical and metabolic imaging studies, known as pseudoprogression.

Performance of a fully-automated Lumipulse plasma phospho-tau181 assay for Alzheimer's disease.

Background: The recent promise of disease-modifying therapies for Alzheimer's disease (AD) has reinforced the need for accurate biomarkers for early disease detection, diagnosis and treatment monitoring. Advances in the development of novel blood-based biomarkers for AD have revealed that plasma levels of tau phosphorylated at various residues are specific and sensitive to AD dementia. However, the currently available tests have shortcomings in access, throughput, and scalability that limit widespread implementation.

Piceatannol extends the lifespan of Caenorhabditis elegans via DAF-16.

Piceatannol is a natural stilbene with many beneficial effects, such as antioxidative, anti-inflammatory, antiatherogenic activities; however, its role on aging is not known. In this study, we used Caenorhabditis elegans as an animal model to study the effect of piceatannol on its lifespan and investigated the underlying mechanisms. The results showed that 50 and 100 µM piceatannol significantly extended the lifespan of C.