Basic Science and Pathogenesis.

Background: Brain accumulation of amyloid-ß (Aß) in plaques and neurons is the cause of AD neuropathology that is opposed by autologous monocyte/macrophages (MMs) in health but this defense fails in AD.

Method: RNAseq, immunochemistry of the brain, immunofluorescence, and confocal microscopy of macrophages.

Result: In the AD brain, MMs shuttle Aß from parenchyma to vessels, which develop vasculitis, causing amyloid-related imaging abnormalities (ARIAs).

Basic Science and Pathogenesis.

Background: Although high-throughput DNA/RNA sequencing technologies have generated massive genetic and genomic data in human disease, translation of these findings into new patient treatment has not materialized by lack of effective approaches, such as Artificial Intelligence (AL) and Machine Learning (ML) tools.

Method: To address this problem, we have used AI/ML approaches, Mendelian randomization (MR), and large patient's genetic and functional genomic data to evaluate druggable targets using Alzheimer's disease (AD) as a prototypical example. We utilized the genomic instruments from 9 expression quantitative trait loci (eQTL) and 3 protein quantitative trait loci (pQTL) datasets across five human brain regions from three biobanks.

Basic Science and Pathogenesis.

Background: Inflammation is crucial in Alzheimer's Disease (AD), where oxidized lipid derivatives of polyunsaturated fatty acids (PUFAs), i.e., oxylipins, are potent modulators.

Insights from a year of field deployments inform the conservation of an endangered estuarine fish.

Freshwater fishes are increasingly facing extinction. Some species will require conservation intervention such as habitat restoration and/or population supplementation through mass-release of hatchery fish. In California, USA, a number of conservation strategies are underway to increase abundance of the endangered Delta Smelt (); however, it is unclear how different estuarine conditions influence hatchery fish.

Strategies for the Immobilization and Signal Amplification of a Double Nanobody Sandwich ELISA for Human Microsomal Epoxide Hydrolase.

The microsomal epoxide hydrolase (mEH) is important in the detoxification of carcinogens in the liver and other tissues but is also a blood biomarker of hepatitis and liver cancer. Improved analytical methods are needed for the study of its role in the metabolism of xenobiotics and endogenous roles as a blood biomarker of diseases. The development of a double nanobody sandwich ELISA offers significant improvements over traditional polyclonal or monoclonal antibody-based assays, enhancing both the homogeneity and the stability of assay production.