Alzheimer’s Disease (AD) is a type of dementia which induces progressive and non-reversible brain disorders (memory and cognitive loss, thinking and behavior changes…). AD ultimately ends in severe mental dysfunction due to neuronal death and breakdown of neural connections. The majority of people with AD are 65+ (late-onset AD). Even if age is one of the greatest risk factors, >5% of AD patients are in their 40s or 50s (early onset AD) making genes and heredityother important AD risk factors (1-4). 

Mitochondria and their functional status provide an early indication of cellular toxicity and thus have emerged as a critical target in drug discovery and toxicity profiling. Apoptosis, necrosis and slow degenerative disease all exhibit changes in the electrochemical gradient across the mitochondrial membranes, ΔΨm, which give rise to the creation of the electronic potential necessary for ATP production.

The transition from non-invasive phenotype to invasive phenotype of tumor cells marks the switch from a benign tumor to a more malignant form of cancer. Understanding the mechanisms underlying this hallmark event, which enables tumor cells to invade through Extracellular matrix, is critical for discovering pathways and new targets to develop anti-metastatic strategies. The discovery of anti-metastatic agents that inhibit cancer cell motility has been hindered by a dearth of cell motility assays that are compatible with high–throughput screening.

The availability of human peripheral blood mononuclear cells (PBMC) from healthy individuals and from patients with various diseases allows for many studies on normal and abnormal functions of human immune cells. Because human and murine immune biology differs in many ways, it is important that various methodologies for studying human immunology are established. The two reports highlighted below demonstrate the usage of human PBMCs for mechanistic and pre-clinical human immune cell studies.