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Alzheimer’s disease and related dementias do not only affect brain neural cells—they also damage the brain’s blood vessels and the protective barrier that separates the brain from the rest of the body, known as the blood–brain barrier. Early in the disease, abnormal buildups of proteins called amyloid beta and tau can accumulate around brain blood vessels. This puts stress on the cells that line these vessels, weakens the blood–brain barrier, and interferes with the brain’s ability to clear toxic substances. These changes can speed up brain inflammation, nerve cell damage, and memory loss.

Despite their importance, the exact ways in which amyloid and tau harm brain blood vessels are not fully understood, and effective treatments targeting this damage are still lacking.

Silvia Fossati, PHD, Director, Alzheimer’s Center at Temple will discuss the research being conducted at Temple University that focuses on how amyloid and tau affect the health, energy production, and survival of brain blood vessel cells. This research also tests new treatment approaches aimed at protecting these cells by targeting specific enzymes inside their mitochondria—the structures that provide energy to cells.

Using models of Alzheimer’s disease, Temple University researchers found that amyloid and tau damage mitochondria, trigger harmful inflammation, weaken the blood–brain barrier, and activate cell death pathways. Importantly, blocking certain mitochondrial enzymes, either with specialized drugs or through genetic approaches, prevents much of this damage. These treatments help restore blood–brain barrier function, improve the brain’s ability to clear toxic proteins, and supported overall brain blood vessel health, proving promising for future clinical trials.